TY  - JOUR
AU  - Subotički, Tijana
AU  - Mitrović-Ajtić, Olivera
AU  - Beleslin-Čokić, Bojana
AU  - Nienhold, Ronny
AU  - Diklić, Miloš
AU  - Đikić, Dragoslava
AU  - Leković, Danijela
AU  - Bulat, Tanja
AU  - Marković, Dragana
AU  - Gotić, Mirjana
AU  - Noguchi, Constance T.
AU  - Schechter, Alan N.
AU  - Skoda, Radek C.
AU  - Čokić, Vladan
PY  - 2017
UR  - http://rimi.imi.bg.ac.rs/handle/123456789/807
AB  - It has been shown that angiogenesis and inflammation play an important role in development of most hematological malignancies including the myeloproliferative neoplasm (MPN). The aim of this study was to investigate and correlate the levels of key angiogenic molecules such as hypoxia-inducible factor-1 (HIF-1), vascular endothelial growth factor (VEGF) and endothelial nitric oxide synthase (eNOS) in peripheral blood and bone marrow cells of MPN patients, along with JAK2V617F mutation allele burden and effects of therapy. HIF-1 and VEGF gene expression were decreased, while eNOS mRNA levels were increased in granulocytes of MPN patients. Furthermore, positively correlated and increased VEGF and eNOS protein levels were in negative correlation with HIF-1 levels in granulocytes of MPN patients. According to immunoblotting, the generally augmented angiogenic factors demonstrated JAK2V617F allele burden dependence only in granulocytes of PMF. The angiogenic factors were largely reduced after hydroxyurea therapy in granulocytes of MPN patients. Levels of eNOS protein expression were stimulated by Calreticulin mutations in granulocytes of essential thrombocythemia. Immunocytochemical analyses of CD34(+) cells showed a more pronounced enhancement of angiogenic factors than in granulocytes. Increased gene expression linked to the proinflammatory TGF and MAPK signaling pathways were detected in CD34(+) cells of MPN patients. In conclusion, the angiogenesis is increased in several cell types of MPN patients supported by the transcriptional activation of inflammation-related target genes, and is not limited to bone marrow stroma cells. It also appears that some of the benefit of hydroxyurea therapy of the MPN is mediated by effects on angiogenic factors.
PB  - Wiley-Blackwell, Hoboken
T2  - Molecular Carcinogenesis
T1  - Angiogenic factors are increased in circulating granulocytes and CD34(+) cells of myeloproliferative neoplasms
EP  - 579
IS  - 2
SP  - 567
VL  - 56
DO  - 10.1002/mc.22517
ER  - 

@article{
author = "Subotički, Tijana and Mitrović-Ajtić, Olivera and Beleslin-Čokić, Bojana and Nienhold, Ronny and Diklić, Miloš and Đikić, Dragoslava and Leković, Danijela and Bulat, Tanja and Marković, Dragana and Gotić, Mirjana and Noguchi, Constance T. and Schechter, Alan N. and Skoda, Radek C. and Čokić, Vladan",
year = "2017",
abstract = "It has been shown that angiogenesis and inflammation play an important role in development of most hematological malignancies including the myeloproliferative neoplasm (MPN). The aim of this study was to investigate and correlate the levels of key angiogenic molecules such as hypoxia-inducible factor-1 (HIF-1), vascular endothelial growth factor (VEGF) and endothelial nitric oxide synthase (eNOS) in peripheral blood and bone marrow cells of MPN patients, along with JAK2V617F mutation allele burden and effects of therapy. HIF-1 and VEGF gene expression were decreased, while eNOS mRNA levels were increased in granulocytes of MPN patients. Furthermore, positively correlated and increased VEGF and eNOS protein levels were in negative correlation with HIF-1 levels in granulocytes of MPN patients. According to immunoblotting, the generally augmented angiogenic factors demonstrated JAK2V617F allele burden dependence only in granulocytes of PMF. The angiogenic factors were largely reduced after hydroxyurea therapy in granulocytes of MPN patients. Levels of eNOS protein expression were stimulated by Calreticulin mutations in granulocytes of essential thrombocythemia. Immunocytochemical analyses of CD34(+) cells showed a more pronounced enhancement of angiogenic factors than in granulocytes. Increased gene expression linked to the proinflammatory TGF and MAPK signaling pathways were detected in CD34(+) cells of MPN patients. In conclusion, the angiogenesis is increased in several cell types of MPN patients supported by the transcriptional activation of inflammation-related target genes, and is not limited to bone marrow stroma cells. It also appears that some of the benefit of hydroxyurea therapy of the MPN is mediated by effects on angiogenic factors.",
publisher = "Wiley-Blackwell, Hoboken",
journal = "Molecular Carcinogenesis",
title = "Angiogenic factors are increased in circulating granulocytes and CD34(+) cells of myeloproliferative neoplasms",
pages = "579-567",
number = "2",
volume = "56",
doi = "10.1002/mc.22517"
}

Subotički, T., Mitrović-Ajtić, O., Beleslin-Čokić, B., Nienhold, R., Diklić, M., Đikić, D., Leković, D., Bulat, T., Marković, D., Gotić, M., Noguchi, C. T., Schechter, A. N., Skoda, R. C.,& Čokić, V.. (2017). Angiogenic factors are increased in circulating granulocytes and CD34(+) cells of myeloproliferative neoplasms. in Molecular Carcinogenesis
Wiley-Blackwell, Hoboken., 56(2), 567-579.
https://doi.org/10.1002/mc.22517

Subotički T, Mitrović-Ajtić O, Beleslin-Čokić B, Nienhold R, Diklić M, Đikić D, Leković D, Bulat T, Marković D, Gotić M, Noguchi CT, Schechter AN, Skoda RC, Čokić V. Angiogenic factors are increased in circulating granulocytes and CD34(+) cells of myeloproliferative neoplasms. in Molecular Carcinogenesis. 2017;56(2):567-579.
doi:10.1002/mc.22517 .

Subotički, Tijana, Mitrović-Ajtić, Olivera, Beleslin-Čokić, Bojana, Nienhold, Ronny, Diklić, Miloš, Đikić, Dragoslava, Leković, Danijela, Bulat, Tanja, Marković, Dragana, Gotić, Mirjana, Noguchi, Constance T., Schechter, Alan N., Skoda, Radek C., Čokić, Vladan, "Angiogenic factors are increased in circulating granulocytes and CD34(+) cells of myeloproliferative neoplasms" in Molecular Carcinogenesis, 56, no. 2 (2017):567-579,
https://doi.org/10.1002/mc.22517 . .

TY  - JOUR
AU  - Čokić, Vladan
AU  - Mossuz, Pascal
AU  - Han, Jing
AU  - Socoro, Nuria
AU  - Beleslin-Čokić, Bojana
AU  - Mitrović, Olivera
AU  - Subotički, Tijana
AU  - Diklić, Miloš
AU  - Leković, Danijela
AU  - Gotić, Mirjana
AU  - Puri, Raj K.
AU  - Noguchi, Constance T.
AU  - Schechter, Alan N.
PY  - 2015
UR  - http://rimi.imi.bg.ac.rs/handle/123456789/670
AB  - The gene and protein expression profiles in myeloproliferative neoplasms (MPNs) may reveal gene and protein markers of a potential clinical relevance in diagnosis, treatment and prediction of response to therapy. Using cDNA microarray analysis of 25,100 unique genes, we studied the gene expression profile of CD34(+) cells and granulocytes obtained from peripheral blood of subjects with essential thrombocythemia (ET), polycythemia vera (PV) and primary myelofibrosis (PMF). The microarray analyses of the CD34(+) cells and granulocytes were performed from 20 de novo MPN subjects: JAK2 positive ET, PV, PMF subjects, and JAK2 negative ET/PMF subjects. The granulocytes for proteomic studies were pooled in 4 groups: PV with JAK2 mutant allele burden above 80%, ET with JAK2 mutation, PMF with JAK2 mutation and ET/PMF with no JAK2 mutation. The number of differentially regulated genes was about two fold larger in CD34(+) cells compared to granulocytes. Thirty-six genes (including RUNX1, TNFRSF19) were persistently highly expressed, while 42 genes (including FOXD4, PDE4A) were underexpressed both in CD34(+) cells and granulocytes. Using proteomic studies, significant up-regulation was observed for MAPK and PI3K/AKT signaling regulators that control myeloid cell apoptosis and proliferation: RAC2, MNDA, S100A8/9, CORO1A, and GNAI2. When the status of the mTOR signaling pathway related genes was analyzed, PI3K/AKT regulators were preferentially up-regulated in CD34(+) cells of MPNs, with down-regulated major components of the protein complex EIF4F. Molecular profiling of CD34(+) cells and granulocytes of MPN determined gene expression patterns beyond their recognized function in disease pathogenesis that included dominant up-regulation of PI3K/AKT signaling.
PB  - Public Library Science, San Francisco
T2  - PLoS One
T1  - Microarray and Proteomic Analyses of Myeloproliferative Neoplasms with a Highlight on the mTOR Signaling Pathway
IS  - 8
VL  - 10
DO  - 10.1371/journal.pone.0135463
ER  - 

@article{
author = "Čokić, Vladan and Mossuz, Pascal and Han, Jing and Socoro, Nuria and Beleslin-Čokić, Bojana and Mitrović, Olivera and Subotički, Tijana and Diklić, Miloš and Leković, Danijela and Gotić, Mirjana and Puri, Raj K. and Noguchi, Constance T. and Schechter, Alan N.",
year = "2015",
abstract = "The gene and protein expression profiles in myeloproliferative neoplasms (MPNs) may reveal gene and protein markers of a potential clinical relevance in diagnosis, treatment and prediction of response to therapy. Using cDNA microarray analysis of 25,100 unique genes, we studied the gene expression profile of CD34(+) cells and granulocytes obtained from peripheral blood of subjects with essential thrombocythemia (ET), polycythemia vera (PV) and primary myelofibrosis (PMF). The microarray analyses of the CD34(+) cells and granulocytes were performed from 20 de novo MPN subjects: JAK2 positive ET, PV, PMF subjects, and JAK2 negative ET/PMF subjects. The granulocytes for proteomic studies were pooled in 4 groups: PV with JAK2 mutant allele burden above 80%, ET with JAK2 mutation, PMF with JAK2 mutation and ET/PMF with no JAK2 mutation. The number of differentially regulated genes was about two fold larger in CD34(+) cells compared to granulocytes. Thirty-six genes (including RUNX1, TNFRSF19) were persistently highly expressed, while 42 genes (including FOXD4, PDE4A) were underexpressed both in CD34(+) cells and granulocytes. Using proteomic studies, significant up-regulation was observed for MAPK and PI3K/AKT signaling regulators that control myeloid cell apoptosis and proliferation: RAC2, MNDA, S100A8/9, CORO1A, and GNAI2. When the status of the mTOR signaling pathway related genes was analyzed, PI3K/AKT regulators were preferentially up-regulated in CD34(+) cells of MPNs, with down-regulated major components of the protein complex EIF4F. Molecular profiling of CD34(+) cells and granulocytes of MPN determined gene expression patterns beyond their recognized function in disease pathogenesis that included dominant up-regulation of PI3K/AKT signaling.",
publisher = "Public Library Science, San Francisco",
journal = "PLoS One",
title = "Microarray and Proteomic Analyses of Myeloproliferative Neoplasms with a Highlight on the mTOR Signaling Pathway",
number = "8",
volume = "10",
doi = "10.1371/journal.pone.0135463"
}

Čokić, V., Mossuz, P., Han, J., Socoro, N., Beleslin-Čokić, B., Mitrović, O., Subotički, T., Diklić, M., Leković, D., Gotić, M., Puri, R. K., Noguchi, C. T.,& Schechter, A. N.. (2015). Microarray and Proteomic Analyses of Myeloproliferative Neoplasms with a Highlight on the mTOR Signaling Pathway. in PLoS One
Public Library Science, San Francisco., 10(8).
https://doi.org/10.1371/journal.pone.0135463

Čokić V, Mossuz P, Han J, Socoro N, Beleslin-Čokić B, Mitrović O, Subotički T, Diklić M, Leković D, Gotić M, Puri RK, Noguchi CT, Schechter AN. Microarray and Proteomic Analyses of Myeloproliferative Neoplasms with a Highlight on the mTOR Signaling Pathway. in PLoS One. 2015;10(8).
doi:10.1371/journal.pone.0135463 .

Čokić, Vladan, Mossuz, Pascal, Han, Jing, Socoro, Nuria, Beleslin-Čokić, Bojana, Mitrović, Olivera, Subotički, Tijana, Diklić, Miloš, Leković, Danijela, Gotić, Mirjana, Puri, Raj K., Noguchi, Constance T., Schechter, Alan N., "Microarray and Proteomic Analyses of Myeloproliferative Neoplasms with a Highlight on the mTOR Signaling Pathway" in PLoS One, 10, no. 8 (2015),
https://doi.org/10.1371/journal.pone.0135463 . .

TY  - JOUR
AU  - Čokić, Vladan
AU  - Smith, Reginald D.
AU  - Biancotto, Angelique
AU  - Noguchi, Constance T.
AU  - Puri, Raj K.
AU  - Schechter, Alan N.
PY  - 2013
UR  - http://rimi.imi.bg.ac.rs/handle/123456789/509
AB  - Background: The guanine nucleotide binding protein (G protein)-coupled receptors (GPCRs) regulate cell growth, proliferation and differentiation. G proteins are also implicated in erythroid differentiation, and some of them are expressed principally in hematopoietic cells. GPCRs-linked NO/cGMP and p38 MAPK signaling pathways already demonstrated potency for globin gene stimulation. By analyzing erythroid progenitors, derived from hematopoietic cells through in vitro ontogeny, our study intends to determine early markers and signaling pathways of globin gene regulation and their relation to GPCR expression. Results: Human hematopoietic CD34(+) progenitors are isolated from fetal liver (FL), cord blood (CB), adult bone marrow (BM), peripheral blood (PB) and G-CSF stimulated mobilized PB (mPB), and then differentiated in vitro into erythroid progenitors. We find that growth capacity is most abundant in FL- and CB-derived erythroid cells. The erythroid progenitor cells are sorted as 100% CD71(+), but we did not find statistical significance in the variations of CD34, CD36 and GlyA antigens and that confirms similarity in maturation of studied ontogenic periods. During ontogeny, beta-globin gene expression reaches maximum levels in cells of adult blood origin (176 fmol/mu g), while gamma-globin gene expression is consistently up-regulated in CB-derived cells (60 fmol/mu g). During gamma-globin induction by hydroxycarbamide, we identify stimulated GPCRs (PTGDR, PTGER1) and GPCRs-coupled genes known to be activated via the cAMP/PKA (ADIPOQ), MAPK pathway (JUN) and NO/cGMP (PRPF18) signaling pathways. During ontogeny, GPR45 and ARRDC1 genes have the most prominent expression in FL-derived erythroid progenitor cells, GNL3 and GRP65 genes in CB-derived cells (high gamma-globin gene expression), GPR110 and GNG10 in BM-derived cells, GPR89C and GPR172A in PB-derived cells, and GPR44 and GNAQ genes in mPB-derived cells (high beta-globin gene expression). Conclusions: These results demonstrate the concomitant activity of GPCR-coupled genes and related signaling pathways during erythropoietic stimulation of globin genes. In accordance with previous reports, the stimulation of GPCRs supports the postulated connection between cAMP/PKA and NO/cGMP pathways in activation of.-globin expression, via JUN and p38 MAPK signaling.
PB  - Biomed Central Ltd, London
T2  - BMC Genomics
T1  - Globin gene expression in correlation with G protein-related genes during erythroid differentiation
VL  - 14
DO  - 10.1186/1471-2164-14-116
ER  - 

@article{
author = "Čokić, Vladan and Smith, Reginald D. and Biancotto, Angelique and Noguchi, Constance T. and Puri, Raj K. and Schechter, Alan N.",
year = "2013",
abstract = "Background: The guanine nucleotide binding protein (G protein)-coupled receptors (GPCRs) regulate cell growth, proliferation and differentiation. G proteins are also implicated in erythroid differentiation, and some of them are expressed principally in hematopoietic cells. GPCRs-linked NO/cGMP and p38 MAPK signaling pathways already demonstrated potency for globin gene stimulation. By analyzing erythroid progenitors, derived from hematopoietic cells through in vitro ontogeny, our study intends to determine early markers and signaling pathways of globin gene regulation and their relation to GPCR expression. Results: Human hematopoietic CD34(+) progenitors are isolated from fetal liver (FL), cord blood (CB), adult bone marrow (BM), peripheral blood (PB) and G-CSF stimulated mobilized PB (mPB), and then differentiated in vitro into erythroid progenitors. We find that growth capacity is most abundant in FL- and CB-derived erythroid cells. The erythroid progenitor cells are sorted as 100% CD71(+), but we did not find statistical significance in the variations of CD34, CD36 and GlyA antigens and that confirms similarity in maturation of studied ontogenic periods. During ontogeny, beta-globin gene expression reaches maximum levels in cells of adult blood origin (176 fmol/mu g), while gamma-globin gene expression is consistently up-regulated in CB-derived cells (60 fmol/mu g). During gamma-globin induction by hydroxycarbamide, we identify stimulated GPCRs (PTGDR, PTGER1) and GPCRs-coupled genes known to be activated via the cAMP/PKA (ADIPOQ), MAPK pathway (JUN) and NO/cGMP (PRPF18) signaling pathways. During ontogeny, GPR45 and ARRDC1 genes have the most prominent expression in FL-derived erythroid progenitor cells, GNL3 and GRP65 genes in CB-derived cells (high gamma-globin gene expression), GPR110 and GNG10 in BM-derived cells, GPR89C and GPR172A in PB-derived cells, and GPR44 and GNAQ genes in mPB-derived cells (high beta-globin gene expression). Conclusions: These results demonstrate the concomitant activity of GPCR-coupled genes and related signaling pathways during erythropoietic stimulation of globin genes. In accordance with previous reports, the stimulation of GPCRs supports the postulated connection between cAMP/PKA and NO/cGMP pathways in activation of.-globin expression, via JUN and p38 MAPK signaling.",
publisher = "Biomed Central Ltd, London",
journal = "BMC Genomics",
title = "Globin gene expression in correlation with G protein-related genes during erythroid differentiation",
volume = "14",
doi = "10.1186/1471-2164-14-116"
}

Čokić, V., Smith, R. D., Biancotto, A., Noguchi, C. T., Puri, R. K.,& Schechter, A. N.. (2013). Globin gene expression in correlation with G protein-related genes during erythroid differentiation. in BMC Genomics
Biomed Central Ltd, London., 14.
https://doi.org/10.1186/1471-2164-14-116

Čokić V, Smith RD, Biancotto A, Noguchi CT, Puri RK, Schechter AN. Globin gene expression in correlation with G protein-related genes during erythroid differentiation. in BMC Genomics. 2013;14.
doi:10.1186/1471-2164-14-116 .

Čokić, Vladan, Smith, Reginald D., Biancotto, Angelique, Noguchi, Constance T., Puri, Raj K., Schechter, Alan N., "Globin gene expression in correlation with G protein-related genes during erythroid differentiation" in BMC Genomics, 14 (2013),
https://doi.org/10.1186/1471-2164-14-116 . .

TY  - JOUR
AU  - Čokić, Vladan
AU  - Bhattacharya, Bhaskar
AU  - Beleslin-Čokić, Bojana
AU  - Noguchi, Constance T.
AU  - Puri, Raj K.
AU  - Schechter, Alan N.
PY  - 2012
UR  - http://rimi.imi.bg.ac.rs/handle/123456789/422
AB  - Background: It has been reported that the phosphatidylinositol 3-kinase (PI3K)-AKT signaling pathway regulates erythropoietin (EPO)-induced survival, proliferation, and maturation of early erythroid progenitors. Erythroid cell proliferation and survival have also been related to activation of the JAK-STAT pathway. The goal of this study was to observe the function of EPO activation of JAK-STAT and PI3K/AKT pathways in the development of erythroid progenitors from hematopoietic CD34(+) progenitor cells, as well as to distinguish early EPO target genes in human erythroid progenitors during ontogeny. Methods: Hematopoietic CD34(+) progenitor cells, isolated from fetal and adult hematopoietic tissues, were differentiated into erythroid progenitor cells. We have used microarray analysis to examine JAK-STAT and PI3K/AKT related genes, as well as broad gene expression modulation in these human erythroid progenitor cells. Results: In microarray studies, a total of 1755 genes were expressed in fetal liver, 3844 in cord blood, 1770 in adult bone marrow, and 1325 genes in peripheral blood-derived erythroid progenitor cells. The erythroid progenitor cells shared 1011 common genes. Using the Ingenuity Pathways Analysis software, we evaluated the network pathways of genes linked to hematological system development, cellular growth and proliferation. The KITLG, EPO, GATA1, PIM1 and STAT3 genes represent the major connection points in the hematological system development linked genes. Some JAK-STAT signaling pathway-linked genes were steadily upregulated throughout ontogeny (PIM1, SOCS2, MYC, PTPN11), while others were downregulated (PTPN6, PIAS, SPRED2). In addition, some JAK-STAT pathway related genes are differentially expressed only in some stages of ontogeny (STATs, GRB2, CREBB). Beside the continuously upregulated (AKT1, PPP2CA, CHUK, NFKB1) and downregulated (FOXO1, PDPK1, PIK3CG) genes in the PI3K-AKT signaling pathway, we also observed intermittently regulated gene expression (NFKBIA, YWHAH). Conclusions: This broad overview of gene expression in erythropoiesis revealed transcription factors differentially expressed in some stages of ontogenesis. Finally, our results show that EPO-mediated proliferation and survival of erythroid progenitors occurs mainly through modulation of JAK-STAT pathway associated STATs, GRB2 and PIK3 genes, as well as AKT pathway-coupled NFKBIA and YWHAH genes.
PB  - BMC, London
T2  - Journal of Translational Medicine
T1  - JAK-STAT and AKT pathway-coupled genes in erythroid progenitor cells through ontogeny
VL  - 10
DO  - 10.1186/1479-5876-10-116
ER  - 

@article{
author = "Čokić, Vladan and Bhattacharya, Bhaskar and Beleslin-Čokić, Bojana and Noguchi, Constance T. and Puri, Raj K. and Schechter, Alan N.",
year = "2012",
abstract = "Background: It has been reported that the phosphatidylinositol 3-kinase (PI3K)-AKT signaling pathway regulates erythropoietin (EPO)-induced survival, proliferation, and maturation of early erythroid progenitors. Erythroid cell proliferation and survival have also been related to activation of the JAK-STAT pathway. The goal of this study was to observe the function of EPO activation of JAK-STAT and PI3K/AKT pathways in the development of erythroid progenitors from hematopoietic CD34(+) progenitor cells, as well as to distinguish early EPO target genes in human erythroid progenitors during ontogeny. Methods: Hematopoietic CD34(+) progenitor cells, isolated from fetal and adult hematopoietic tissues, were differentiated into erythroid progenitor cells. We have used microarray analysis to examine JAK-STAT and PI3K/AKT related genes, as well as broad gene expression modulation in these human erythroid progenitor cells. Results: In microarray studies, a total of 1755 genes were expressed in fetal liver, 3844 in cord blood, 1770 in adult bone marrow, and 1325 genes in peripheral blood-derived erythroid progenitor cells. The erythroid progenitor cells shared 1011 common genes. Using the Ingenuity Pathways Analysis software, we evaluated the network pathways of genes linked to hematological system development, cellular growth and proliferation. The KITLG, EPO, GATA1, PIM1 and STAT3 genes represent the major connection points in the hematological system development linked genes. Some JAK-STAT signaling pathway-linked genes were steadily upregulated throughout ontogeny (PIM1, SOCS2, MYC, PTPN11), while others were downregulated (PTPN6, PIAS, SPRED2). In addition, some JAK-STAT pathway related genes are differentially expressed only in some stages of ontogeny (STATs, GRB2, CREBB). Beside the continuously upregulated (AKT1, PPP2CA, CHUK, NFKB1) and downregulated (FOXO1, PDPK1, PIK3CG) genes in the PI3K-AKT signaling pathway, we also observed intermittently regulated gene expression (NFKBIA, YWHAH). Conclusions: This broad overview of gene expression in erythropoiesis revealed transcription factors differentially expressed in some stages of ontogenesis. Finally, our results show that EPO-mediated proliferation and survival of erythroid progenitors occurs mainly through modulation of JAK-STAT pathway associated STATs, GRB2 and PIK3 genes, as well as AKT pathway-coupled NFKBIA and YWHAH genes.",
publisher = "BMC, London",
journal = "Journal of Translational Medicine",
title = "JAK-STAT and AKT pathway-coupled genes in erythroid progenitor cells through ontogeny",
volume = "10",
doi = "10.1186/1479-5876-10-116"
}

Čokić, V., Bhattacharya, B., Beleslin-Čokić, B., Noguchi, C. T., Puri, R. K.,& Schechter, A. N.. (2012). JAK-STAT and AKT pathway-coupled genes in erythroid progenitor cells through ontogeny. in Journal of Translational Medicine
BMC, London., 10.
https://doi.org/10.1186/1479-5876-10-116

Čokić V, Bhattacharya B, Beleslin-Čokić B, Noguchi CT, Puri RK, Schechter AN. JAK-STAT and AKT pathway-coupled genes in erythroid progenitor cells through ontogeny. in Journal of Translational Medicine. 2012;10.
doi:10.1186/1479-5876-10-116 .

Čokić, Vladan, Bhattacharya, Bhaskar, Beleslin-Čokić, Bojana, Noguchi, Constance T., Puri, Raj K., Schechter, Alan N., "JAK-STAT and AKT pathway-coupled genes in erythroid progenitor cells through ontogeny" in Journal of Translational Medicine, 10 (2012),
https://doi.org/10.1186/1479-5876-10-116 . .

TY  - CONF
AU  - Čokić, Vladan
AU  - Mossuz, Pascal
AU  - Sefer, Dijana
AU  - Diklić, Miloš
AU  - Breković, Tijana
AU  - Vignjević, Sanja
AU  - Ilić, B.
AU  - Noguchi, Constance T.
AU  - Schechter, Alan N.
PY  - 2012
UR  - http://rimi.imi.bg.ac.rs/handle/123456789/436
PB  - Ferrata Storti Foundation, Pavia
C3  - Haematologica
T1  - Expression analysis of s100 proteins in myeloproliferative neoplasm by microarray and proteomic studies
EP  - 380
SP  - 380
VL  - 97
UR  - https://hdl.handle.net/21.15107/rcub_rimi_436
ER  - 

@conference{
author = "Čokić, Vladan and Mossuz, Pascal and Sefer, Dijana and Diklić, Miloš and Breković, Tijana and Vignjević, Sanja and Ilić, B. and Noguchi, Constance T. and Schechter, Alan N.",
year = "2012",
publisher = "Ferrata Storti Foundation, Pavia",
journal = "Haematologica",
title = "Expression analysis of s100 proteins in myeloproliferative neoplasm by microarray and proteomic studies",
pages = "380-380",
volume = "97",
url = "https://hdl.handle.net/21.15107/rcub_rimi_436"
}

Čokić, V., Mossuz, P., Sefer, D., Diklić, M., Breković, T., Vignjević, S., Ilić, B., Noguchi, C. T.,& Schechter, A. N.. (2012). Expression analysis of s100 proteins in myeloproliferative neoplasm by microarray and proteomic studies. in Haematologica
Ferrata Storti Foundation, Pavia., 97, 380-380.
https://hdl.handle.net/21.15107/rcub_rimi_436

Čokić V, Mossuz P, Sefer D, Diklić M, Breković T, Vignjević S, Ilić B, Noguchi CT, Schechter AN. Expression analysis of s100 proteins in myeloproliferative neoplasm by microarray and proteomic studies. in Haematologica. 2012;97:380-380.
https://hdl.handle.net/21.15107/rcub_rimi_436 .

Čokić, Vladan, Mossuz, Pascal, Sefer, Dijana, Diklić, Miloš, Breković, Tijana, Vignjević, Sanja, Ilić, B., Noguchi, Constance T., Schechter, Alan N., "Expression analysis of s100 proteins in myeloproliferative neoplasm by microarray and proteomic studies" in Haematologica, 97 (2012):380-380,
https://hdl.handle.net/21.15107/rcub_rimi_436 .

TY  - CONF
AU  - Čokić, Vladan
AU  - Marković, Dragana
AU  - Mitrović, Olivera
AU  - Vignjević, Sanja
AU  - Đikić, Dragoslava
AU  - Beleslin-Čokić, Bojana
AU  - Peruničić, Maja
AU  - Ilić, Bojana
AU  - Jovčić, Gordana
AU  - Gotić, Mirjana
AU  - Noguchi, Constance T.
AU  - Schechter, Alan N.
PY  - 2011
UR  - http://rimi.imi.bg.ac.rs/handle/123456789/349
PB  - Amer Soc Hematology, Washington
C3  - Blood
T1  - Angiogenic Factors eNOS and VEGF Have Increased Expression in Granulocytes of JAK2V617F Homozygous Forms of Polycythemia Vera
EP  - 1645
IS  - 21
SP  - 1645
VL  - 118
UR  - https://hdl.handle.net/21.15107/rcub_rimi_349
ER  - 

@conference{
author = "Čokić, Vladan and Marković, Dragana and Mitrović, Olivera and Vignjević, Sanja and Đikić, Dragoslava and Beleslin-Čokić, Bojana and Peruničić, Maja and Ilić, Bojana and Jovčić, Gordana and Gotić, Mirjana and Noguchi, Constance T. and Schechter, Alan N.",
year = "2011",
publisher = "Amer Soc Hematology, Washington",
journal = "Blood",
title = "Angiogenic Factors eNOS and VEGF Have Increased Expression in Granulocytes of JAK2V617F Homozygous Forms of Polycythemia Vera",
pages = "1645-1645",
number = "21",
volume = "118",
url = "https://hdl.handle.net/21.15107/rcub_rimi_349"
}

Čokić, V., Marković, D., Mitrović, O., Vignjević, S., Đikić, D., Beleslin-Čokić, B., Peruničić, M., Ilić, B., Jovčić, G., Gotić, M., Noguchi, C. T.,& Schechter, A. N.. (2011). Angiogenic Factors eNOS and VEGF Have Increased Expression in Granulocytes of JAK2V617F Homozygous Forms of Polycythemia Vera. in Blood
Amer Soc Hematology, Washington., 118(21), 1645-1645.
https://hdl.handle.net/21.15107/rcub_rimi_349

Čokić V, Marković D, Mitrović O, Vignjević S, Đikić D, Beleslin-Čokić B, Peruničić M, Ilić B, Jovčić G, Gotić M, Noguchi CT, Schechter AN. Angiogenic Factors eNOS and VEGF Have Increased Expression in Granulocytes of JAK2V617F Homozygous Forms of Polycythemia Vera. in Blood. 2011;118(21):1645-1645.
https://hdl.handle.net/21.15107/rcub_rimi_349 .

Čokić, Vladan, Marković, Dragana, Mitrović, Olivera, Vignjević, Sanja, Đikić, Dragoslava, Beleslin-Čokić, Bojana, Peruničić, Maja, Ilić, Bojana, Jovčić, Gordana, Gotić, Mirjana, Noguchi, Constance T., Schechter, Alan N., "Angiogenic Factors eNOS and VEGF Have Increased Expression in Granulocytes of JAK2V617F Homozygous Forms of Polycythemia Vera" in Blood, 118, no. 21 (2011):1645-1645,
https://hdl.handle.net/21.15107/rcub_rimi_349 .

TY  - CONF
AU  - Čokić, Vladan
AU  - Mossuz, Pascal
AU  - Han, Jing
AU  - Diklić, Miloš
AU  - Budeč, Mirela
AU  - Sefer, Dijana
AU  - Leković, Danijela
AU  - Antić, Darko
AU  - Breković, Tijana
AU  - Mojsilović, Sonja
AU  - Puri, Raj K.
AU  - Noguchi, Constance T.
AU  - Schechter, Alan N.
PY  - 2011
UR  - http://rimi.imi.bg.ac.rs/handle/123456789/348
PB  - Amer Soc Hematology, Washington
C3  - Blood
T1  - Microarray and Proteomic Analysis of Myeloproliferative Neoplasms
EP  - 1649
IS  - 21
SP  - 1649
VL  - 118
UR  - https://hdl.handle.net/21.15107/rcub_rimi_348
ER  - 

@conference{
author = "Čokić, Vladan and Mossuz, Pascal and Han, Jing and Diklić, Miloš and Budeč, Mirela and Sefer, Dijana and Leković, Danijela and Antić, Darko and Breković, Tijana and Mojsilović, Sonja and Puri, Raj K. and Noguchi, Constance T. and Schechter, Alan N.",
year = "2011",
publisher = "Amer Soc Hematology, Washington",
journal = "Blood",
title = "Microarray and Proteomic Analysis of Myeloproliferative Neoplasms",
pages = "1649-1649",
number = "21",
volume = "118",
url = "https://hdl.handle.net/21.15107/rcub_rimi_348"
}

Čokić, V., Mossuz, P., Han, J., Diklić, M., Budeč, M., Sefer, D., Leković, D., Antić, D., Breković, T., Mojsilović, S., Puri, R. K., Noguchi, C. T.,& Schechter, A. N.. (2011). Microarray and Proteomic Analysis of Myeloproliferative Neoplasms. in Blood
Amer Soc Hematology, Washington., 118(21), 1649-1649.
https://hdl.handle.net/21.15107/rcub_rimi_348

Čokić V, Mossuz P, Han J, Diklić M, Budeč M, Sefer D, Leković D, Antić D, Breković T, Mojsilović S, Puri RK, Noguchi CT, Schechter AN. Microarray and Proteomic Analysis of Myeloproliferative Neoplasms. in Blood. 2011;118(21):1649-1649.
https://hdl.handle.net/21.15107/rcub_rimi_348 .

Čokić, Vladan, Mossuz, Pascal, Han, Jing, Diklić, Miloš, Budeč, Mirela, Sefer, Dijana, Leković, Danijela, Antić, Darko, Breković, Tijana, Mojsilović, Sonja, Puri, Raj K., Noguchi, Constance T., Schechter, Alan N., "Microarray and Proteomic Analysis of Myeloproliferative Neoplasms" in Blood, 118, no. 21 (2011):1649-1649,
https://hdl.handle.net/21.15107/rcub_rimi_348 .

TY  - JOUR
AU  - Beleslin-Čokić, Bojana
AU  - Čokić, Vladan
AU  - Wang, Li
AU  - Piknova, Barbora
AU  - Teng, Ruifeng
AU  - Schechter, Alan N.
AU  - Noguchi, Constance T.
PY  - 2011
UR  - http://rimi.imi.bg.ac.rs/handle/123456789/341
AB  - Acute lung exposure to low oxygen results in pulmonary vasoconstriction and redistribution of blood flow. We used human microvascular endothelial cells from lung (HMVEC-L) to study the acute response to oxygen stress. We observed that hypoxia and erythropoietin (EPO) increased erythropoietin receptor (EPOR) gene expression and protein level in HMVEC-L In addition, EPO dose- and time-dependently stimulated nitric oxide (NO) production. This NO stimulation was evident despite hypoxia induced reduction of endothelial NO synthase (eNOS) gene expression. Western blot of phospho-eNOS (serine1177) and eNOS and was significantly induced by hypoxia but not after EPO treatment. However, iNOS increased at hypoxia and with EPO stimulation compared to normal oxygen tension. In accordance with our previous results of NO induction by EPO at low oxygen tension in human umbilical vein endothelial cells and bone marrow endothelial cells, these results provide further evidence in HMVEC-L for EPO regulation of NO production to modify the effects of hypoxia and cause compensatory vasoconstriction.
PB  - Academic Press Ltd- Elsevier Science Ltd, London
T2  - Cytokine
T1  - Erythropoietin and hypoxia increase erythropoietin receptor and nitric oxide levels in lung microvascular endothelial cells
EP  - 135
IS  - 2
SP  - 129
VL  - 54
DO  - 10.1016/j.cyto.2011.01.015
ER  - 

@article{
author = "Beleslin-Čokić, Bojana and Čokić, Vladan and Wang, Li and Piknova, Barbora and Teng, Ruifeng and Schechter, Alan N. and Noguchi, Constance T.",
year = "2011",
abstract = "Acute lung exposure to low oxygen results in pulmonary vasoconstriction and redistribution of blood flow. We used human microvascular endothelial cells from lung (HMVEC-L) to study the acute response to oxygen stress. We observed that hypoxia and erythropoietin (EPO) increased erythropoietin receptor (EPOR) gene expression and protein level in HMVEC-L In addition, EPO dose- and time-dependently stimulated nitric oxide (NO) production. This NO stimulation was evident despite hypoxia induced reduction of endothelial NO synthase (eNOS) gene expression. Western blot of phospho-eNOS (serine1177) and eNOS and was significantly induced by hypoxia but not after EPO treatment. However, iNOS increased at hypoxia and with EPO stimulation compared to normal oxygen tension. In accordance with our previous results of NO induction by EPO at low oxygen tension in human umbilical vein endothelial cells and bone marrow endothelial cells, these results provide further evidence in HMVEC-L for EPO regulation of NO production to modify the effects of hypoxia and cause compensatory vasoconstriction.",
publisher = "Academic Press Ltd- Elsevier Science Ltd, London",
journal = "Cytokine",
title = "Erythropoietin and hypoxia increase erythropoietin receptor and nitric oxide levels in lung microvascular endothelial cells",
pages = "135-129",
number = "2",
volume = "54",
doi = "10.1016/j.cyto.2011.01.015"
}

Beleslin-Čokić, B., Čokić, V., Wang, L., Piknova, B., Teng, R., Schechter, A. N.,& Noguchi, C. T.. (2011). Erythropoietin and hypoxia increase erythropoietin receptor and nitric oxide levels in lung microvascular endothelial cells. in Cytokine
Academic Press Ltd- Elsevier Science Ltd, London., 54(2), 129-135.
https://doi.org/10.1016/j.cyto.2011.01.015

Beleslin-Čokić B, Čokić V, Wang L, Piknova B, Teng R, Schechter AN, Noguchi CT. Erythropoietin and hypoxia increase erythropoietin receptor and nitric oxide levels in lung microvascular endothelial cells. in Cytokine. 2011;54(2):129-135.
doi:10.1016/j.cyto.2011.01.015 .

Beleslin-Čokić, Bojana, Čokić, Vladan, Wang, Li, Piknova, Barbora, Teng, Ruifeng, Schechter, Alan N., Noguchi, Constance T., "Erythropoietin and hypoxia increase erythropoietin receptor and nitric oxide levels in lung microvascular endothelial cells" in Cytokine, 54, no. 2 (2011):129-135,
https://doi.org/10.1016/j.cyto.2011.01.015 . .

TY  - CONF
AU  - Čokić, Vladan
AU  - Mojsilović, S.
AU  - Miloksević, V.
AU  - Kraguljac-Kurtović, Nada
AU  - Bogdanović, Andrija
AU  - Jovčić, Gordana
AU  - Milenković, P.
AU  - Gotić, Mirjana
AU  - Noguchi, Constance T.
AU  - Schechter, Alan N.
PY  - 2010
UR  - http://rimi.imi.bg.ac.rs/handle/123456789/312
PB  - Ferrata Storti Foundation, Pavia
C3  - Haematologica
T1  - Gene expression profile of hematopoietic progenitor cells vs. Granulocytes in chronic myeloid leukemia
EP  - 335
SP  - 334
VL  - 95
UR  - https://hdl.handle.net/21.15107/rcub_rimi_312
ER  - 

@conference{
author = "Čokić, Vladan and Mojsilović, S. and Miloksević, V. and Kraguljac-Kurtović, Nada and Bogdanović, Andrija and Jovčić, Gordana and Milenković, P. and Gotić, Mirjana and Noguchi, Constance T. and Schechter, Alan N.",
year = "2010",
publisher = "Ferrata Storti Foundation, Pavia",
journal = "Haematologica",
title = "Gene expression profile of hematopoietic progenitor cells vs. Granulocytes in chronic myeloid leukemia",
pages = "335-334",
volume = "95",
url = "https://hdl.handle.net/21.15107/rcub_rimi_312"
}

Čokić, V., Mojsilović, S., Miloksević, V., Kraguljac-Kurtović, N., Bogdanović, A., Jovčić, G., Milenković, P., Gotić, M., Noguchi, C. T.,& Schechter, A. N.. (2010). Gene expression profile of hematopoietic progenitor cells vs. Granulocytes in chronic myeloid leukemia. in Haematologica
Ferrata Storti Foundation, Pavia., 95, 334-335.
https://hdl.handle.net/21.15107/rcub_rimi_312

Čokić V, Mojsilović S, Miloksević V, Kraguljac-Kurtović N, Bogdanović A, Jovčić G, Milenković P, Gotić M, Noguchi CT, Schechter AN. Gene expression profile of hematopoietic progenitor cells vs. Granulocytes in chronic myeloid leukemia. in Haematologica. 2010;95:334-335.
https://hdl.handle.net/21.15107/rcub_rimi_312 .

Čokić, Vladan, Mojsilović, S., Miloksević, V., Kraguljac-Kurtović, Nada, Bogdanović, Andrija, Jovčić, Gordana, Milenković, P., Gotić, Mirjana, Noguchi, Constance T., Schechter, Alan N., "Gene expression profile of hematopoietic progenitor cells vs. Granulocytes in chronic myeloid leukemia" in Haematologica, 95 (2010):334-335,
https://hdl.handle.net/21.15107/rcub_rimi_312 .

TY  - CONF
AU  - Čokić, Vladan
AU  - Bhattacharya, Bhaskar
AU  - Beleslin-Čokić, Bojana
AU  - Noguchi, Constance T.
AU  - Puri, Raj K.
AU  - Schechter, Alan N.
PY  - 2010
UR  - http://rimi.imi.bg.ac.rs/handle/123456789/311
PB  - Elsevier Science Inc, New York
C3  - Experimental Hematology
T1  - Globin genes versus common genes expression profiling in erythroid cells during ontogeny
EP  - S29
IS  - 9
SP  - S29
VL  - 38
UR  - https://hdl.handle.net/21.15107/rcub_rimi_311
ER  - 

@conference{
author = "Čokić, Vladan and Bhattacharya, Bhaskar and Beleslin-Čokić, Bojana and Noguchi, Constance T. and Puri, Raj K. and Schechter, Alan N.",
year = "2010",
publisher = "Elsevier Science Inc, New York",
journal = "Experimental Hematology",
title = "Globin genes versus common genes expression profiling in erythroid cells during ontogeny",
pages = "S29-S29",
number = "9",
volume = "38",
url = "https://hdl.handle.net/21.15107/rcub_rimi_311"
}

Čokić, V., Bhattacharya, B., Beleslin-Čokić, B., Noguchi, C. T., Puri, R. K.,& Schechter, A. N.. (2010). Globin genes versus common genes expression profiling in erythroid cells during ontogeny. in Experimental Hematology
Elsevier Science Inc, New York., 38(9), S29-S29.
https://hdl.handle.net/21.15107/rcub_rimi_311

Čokić V, Bhattacharya B, Beleslin-Čokić B, Noguchi CT, Puri RK, Schechter AN. Globin genes versus common genes expression profiling in erythroid cells during ontogeny. in Experimental Hematology. 2010;38(9):S29-S29.
https://hdl.handle.net/21.15107/rcub_rimi_311 .

Čokić, Vladan, Bhattacharya, Bhaskar, Beleslin-Čokić, Bojana, Noguchi, Constance T., Puri, Raj K., Schechter, Alan N., "Globin genes versus common genes expression profiling in erythroid cells during ontogeny" in Experimental Hematology, 38, no. 9 (2010):S29-S29,
https://hdl.handle.net/21.15107/rcub_rimi_311 .

TY  - CONF
AU  - Čokić, Vladan
AU  - Han, Jing
AU  - Beleslin-Čokić, Bojana
AU  - Mirković, K.
AU  - Damjanović, Svetozar
AU  - Gotić, Mirjana
AU  - Raj, Puri K.
AU  - Noguchi, Constance T.
AU  - Schechter, Alan N.
PY  - 2010
UR  - http://rimi.imi.bg.ac.rs/handle/123456789/300
PB  - Ferrata Storti Foundation, Pavia
C3  - Haematologica
T1  - Therapy related gene expression of hematopoietic progenitor cells in chronic myeloproliferative neoplasms
EP  - 403
SP  - 403
VL  - 95
UR  - https://hdl.handle.net/21.15107/rcub_rimi_300
ER  - 

@conference{
author = "Čokić, Vladan and Han, Jing and Beleslin-Čokić, Bojana and Mirković, K. and Damjanović, Svetozar and Gotić, Mirjana and Raj, Puri K. and Noguchi, Constance T. and Schechter, Alan N.",
year = "2010",
publisher = "Ferrata Storti Foundation, Pavia",
journal = "Haematologica",
title = "Therapy related gene expression of hematopoietic progenitor cells in chronic myeloproliferative neoplasms",
pages = "403-403",
volume = "95",
url = "https://hdl.handle.net/21.15107/rcub_rimi_300"
}

Čokić, V., Han, J., Beleslin-Čokić, B., Mirković, K., Damjanović, S., Gotić, M., Raj, P. K., Noguchi, C. T.,& Schechter, A. N.. (2010). Therapy related gene expression of hematopoietic progenitor cells in chronic myeloproliferative neoplasms. in Haematologica
Ferrata Storti Foundation, Pavia., 95, 403-403.
https://hdl.handle.net/21.15107/rcub_rimi_300

Čokić V, Han J, Beleslin-Čokić B, Mirković K, Damjanović S, Gotić M, Raj PK, Noguchi CT, Schechter AN. Therapy related gene expression of hematopoietic progenitor cells in chronic myeloproliferative neoplasms. in Haematologica. 2010;95:403-403.
https://hdl.handle.net/21.15107/rcub_rimi_300 .

Čokić, Vladan, Han, Jing, Beleslin-Čokić, Bojana, Mirković, K., Damjanović, Svetozar, Gotić, Mirjana, Raj, Puri K., Noguchi, Constance T., Schechter, Alan N., "Therapy related gene expression of hematopoietic progenitor cells in chronic myeloproliferative neoplasms" in Haematologica, 95 (2010):403-403,
https://hdl.handle.net/21.15107/rcub_rimi_300 .

TY  - JOUR
AU  - Čokić, Vladan
AU  - Beleslin-Čokić, Bojana
AU  - Smith, Reginald D.
AU  - Economou, Antaeus P.
AU  - Wahl, Larry M.
AU  - Noguchi, Constance T.
AU  - Schechter, Alan N.
PY  - 2009
UR  - http://rimi.imi.bg.ac.rs/handle/123456789/223
AB  - Objective. We have previously shown that nitric oxide (NO) is involved in the hydroxyurea-induced increase of gamma-globin gene expression in cultured human erythroid progenitor cells and that hydroxyurea increases NO production in endothelial cells via endothelial NO synthase (NOS). We have now expanded those studies to demonstrate that stimulation of gamma-globin gene expression is also mediated by NOS induction in stromal cells within the bone marrow microenvironment. Materials and Methods. Using NO analyzer, we measured NO production in endothelial and macrophage cell cultures. In coculture studies of erythroid and stromal cells, we measured globin gene expression during stimulation by NO induers. Results. Hydroxyurea (30 - 100 mu M) induced NOS-dependent production of NO in human macrophages (up to 1.2 mu M). Coculture studies of human macrophages with erythroid progenitor cells also resulted in induction of gamma-globin mRNA expression (up to threefold) in the presence of hydroxyurea. NOS-dependent stimulation of NO by lipopolysaccharide (up to 0.6 mu M) has been observed in human macrophages. We found that lipopolysaccharide and interferon-gamma together increased gamma-globin gene expression (up to twofold) in human macrophage/erythroid cell cocultures. Coculture of human bone marrow endothelial cells with erythroid progenitor cells also induced gamma-globin mRNA expression (2.4-fold) in the presence of hydroxyurea (40 mu M). Conclusion. These results demonstrate an arrangement by which NO and fetal hemoglobin inducers may stimulate globin genes in erythroid cells via the common paracrine effect of bone marrow stromal cells.
PB  - Elsevier Science Inc, New York
T2  - Experimental Hematology
T1  - Stimulated stromal cells induce gamma-globin gene expression in erythroid cells via nitric oxide production
EP  - 1237
IS  - 10
SP  - 1230
VL  - 37
DO  - 10.1016/j.exphem.2009.06.009
ER  - 

@article{
author = "Čokić, Vladan and Beleslin-Čokić, Bojana and Smith, Reginald D. and Economou, Antaeus P. and Wahl, Larry M. and Noguchi, Constance T. and Schechter, Alan N.",
year = "2009",
abstract = "Objective. We have previously shown that nitric oxide (NO) is involved in the hydroxyurea-induced increase of gamma-globin gene expression in cultured human erythroid progenitor cells and that hydroxyurea increases NO production in endothelial cells via endothelial NO synthase (NOS). We have now expanded those studies to demonstrate that stimulation of gamma-globin gene expression is also mediated by NOS induction in stromal cells within the bone marrow microenvironment. Materials and Methods. Using NO analyzer, we measured NO production in endothelial and macrophage cell cultures. In coculture studies of erythroid and stromal cells, we measured globin gene expression during stimulation by NO induers. Results. Hydroxyurea (30 - 100 mu M) induced NOS-dependent production of NO in human macrophages (up to 1.2 mu M). Coculture studies of human macrophages with erythroid progenitor cells also resulted in induction of gamma-globin mRNA expression (up to threefold) in the presence of hydroxyurea. NOS-dependent stimulation of NO by lipopolysaccharide (up to 0.6 mu M) has been observed in human macrophages. We found that lipopolysaccharide and interferon-gamma together increased gamma-globin gene expression (up to twofold) in human macrophage/erythroid cell cocultures. Coculture of human bone marrow endothelial cells with erythroid progenitor cells also induced gamma-globin mRNA expression (2.4-fold) in the presence of hydroxyurea (40 mu M). Conclusion. These results demonstrate an arrangement by which NO and fetal hemoglobin inducers may stimulate globin genes in erythroid cells via the common paracrine effect of bone marrow stromal cells.",
publisher = "Elsevier Science Inc, New York",
journal = "Experimental Hematology",
title = "Stimulated stromal cells induce gamma-globin gene expression in erythroid cells via nitric oxide production",
pages = "1237-1230",
number = "10",
volume = "37",
doi = "10.1016/j.exphem.2009.06.009"
}

Čokić, V., Beleslin-Čokić, B., Smith, R. D., Economou, A. P., Wahl, L. M., Noguchi, C. T.,& Schechter, A. N.. (2009). Stimulated stromal cells induce gamma-globin gene expression in erythroid cells via nitric oxide production. in Experimental Hematology
Elsevier Science Inc, New York., 37(10), 1230-1237.
https://doi.org/10.1016/j.exphem.2009.06.009

Čokić V, Beleslin-Čokić B, Smith RD, Economou AP, Wahl LM, Noguchi CT, Schechter AN. Stimulated stromal cells induce gamma-globin gene expression in erythroid cells via nitric oxide production. in Experimental Hematology. 2009;37(10):1230-1237.
doi:10.1016/j.exphem.2009.06.009 .

Čokić, Vladan, Beleslin-Čokić, Bojana, Smith, Reginald D., Economou, Antaeus P., Wahl, Larry M., Noguchi, Constance T., Schechter, Alan N., "Stimulated stromal cells induce gamma-globin gene expression in erythroid cells via nitric oxide production" in Experimental Hematology, 37, no. 10 (2009):1230-1237,
https://doi.org/10.1016/j.exphem.2009.06.009 . .

TY  - CONF
AU  - Cokić, P.
AU  - Han, Jing
AU  - Mojsilović, S.
AU  - Beleslin-Čokić, Bojana
AU  - Mirković, K.
AU  - Kraguljac-Kurtović, Nada
AU  - Damjanović, Svetozar
AU  - Gotić, Mirjana
AU  - Skoda, R.
AU  - Puri, Raj K.
AU  - Noguchi, Constance T.
AU  - Schechter, Alan N.
PY  - 2009
UR  - http://rimi.imi.bg.ac.rs/handle/123456789/251
PB  - Ferrata Storti Foundation, Pavia
C3  - Haematologica
T1  - Gene expression profiling of cd34(+) cells in myeloproliferative disorders by cdna microarray technology
EP  - 352
SP  - 352
VL  - 94
UR  - https://hdl.handle.net/21.15107/rcub_rimi_251
ER  - 

@conference{
author = "Cokić, P. and Han, Jing and Mojsilović, S. and Beleslin-Čokić, Bojana and Mirković, K. and Kraguljac-Kurtović, Nada and Damjanović, Svetozar and Gotić, Mirjana and Skoda, R. and Puri, Raj K. and Noguchi, Constance T. and Schechter, Alan N.",
year = "2009",
publisher = "Ferrata Storti Foundation, Pavia",
journal = "Haematologica",
title = "Gene expression profiling of cd34(+) cells in myeloproliferative disorders by cdna microarray technology",
pages = "352-352",
volume = "94",
url = "https://hdl.handle.net/21.15107/rcub_rimi_251"
}

Cokić, P., Han, J., Mojsilović, S., Beleslin-Čokić, B., Mirković, K., Kraguljac-Kurtović, N., Damjanović, S., Gotić, M., Skoda, R., Puri, R. K., Noguchi, C. T.,& Schechter, A. N.. (2009). Gene expression profiling of cd34(+) cells in myeloproliferative disorders by cdna microarray technology. in Haematologica
Ferrata Storti Foundation, Pavia., 94, 352-352.
https://hdl.handle.net/21.15107/rcub_rimi_251

Cokić P, Han J, Mojsilović S, Beleslin-Čokić B, Mirković K, Kraguljac-Kurtović N, Damjanović S, Gotić M, Skoda R, Puri RK, Noguchi CT, Schechter AN. Gene expression profiling of cd34(+) cells in myeloproliferative disorders by cdna microarray technology. in Haematologica. 2009;94:352-352.
https://hdl.handle.net/21.15107/rcub_rimi_251 .

Cokić, P., Han, Jing, Mojsilović, S., Beleslin-Čokić, Bojana, Mirković, K., Kraguljac-Kurtović, Nada, Damjanović, Svetozar, Gotić, Mirjana, Skoda, R., Puri, Raj K., Noguchi, Constance T., Schechter, Alan N., "Gene expression profiling of cd34(+) cells in myeloproliferative disorders by cdna microarray technology" in Haematologica, 94 (2009):352-352,
https://hdl.handle.net/21.15107/rcub_rimi_251 .

TY  - JOUR
AU  - Čokić, Vladan
AU  - Schechter, Alan N.
PY  - 2008
UR  - http://rimi.imi.bg.ac.rs/handle/123456789/215
AB  - Nitric oxide (NO) is a diffusible free radical generated primarily by NO synthases (NOS), isoenzymes that convert the l-arginine and molecular oxygen to citrulline and NO in cells. Endothelial cells as well as macrophages, components of hematopoietic microenvironment and potent NO producers, play an active role in the modulation of human hematopoietic cell growth and differentiation. A role of NO in erythroid cell differentiation has been postulated based on demonstration that NO inhibits growth, differentiation, and hemoglobinization of erythroid primary cells. Endothelial NOS (eNOS) mRNA and protein levels, as well as bioactivity, decrease during erythroid differentiation, concomitantly with the elevation of hemoglobin levels. Human red blood cells (RBCs) have been reported to contain some eNOS activity; NO appears to affect RBC's deformability. Generally, NO activates cellular soluble guanylyl cyclase (sGC) to produce a second messenger molecule cGMP. NO increases cGMP, γ-globin, and HbF levels in human erythroid cells whereas inhibition of sGC prevents NO-induced increase in γ-globin gene expression. Activation of sGC increases γ-globin gene expression in primary human erythroblasts. High cAMP levels continuously decrease in contrast to steady but low levels of cGMP during erythroid differentiation. The activation of the cAMP pathway has also been reported to induce expression of the γ-globin gene in human erythroid cells. NO is hydrophobic and accumulates in lipid membranes, and most autoxidation to nitrite in vivo occurs there. The reaction of NO with deoxyhemoglobin produces nitrosylhemoglobin (HbFe(II)NO), while that with oxyhemoglobin produced methemoglobin and nitrate. Nitrite can also react with deoxyhemoglobin to produce NO. This reaction as well as the postulated formation of a thiol-NO derivative of hemoglobin (SNO-Hb) appears to be major mechanisms for the preservation and transport of NO bioactivity by red cells-making NO act as a "hormone." Thus, RBCs and hemoglobin molecules are essential factors in regulating the bioactivity of NO throughout the mammalian body and may be important in the pathophysiology of several circulatory diseases and be the basis for new therapeutic approaches to these diseases. © 2008 Elsevier Inc. All rights reserved.
T2  - Current Topics in Developmental Biology
T1  - Effects of Nitric Oxide on Red Blood Cell Development and Phenotype
EP  - 215
SP  - 169
VL  - 82
DO  - 10.1016/S0070-2153(07)00007-5
ER  - 

@article{
author = "Čokić, Vladan and Schechter, Alan N.",
year = "2008",
abstract = "Nitric oxide (NO) is a diffusible free radical generated primarily by NO synthases (NOS), isoenzymes that convert the l-arginine and molecular oxygen to citrulline and NO in cells. Endothelial cells as well as macrophages, components of hematopoietic microenvironment and potent NO producers, play an active role in the modulation of human hematopoietic cell growth and differentiation. A role of NO in erythroid cell differentiation has been postulated based on demonstration that NO inhibits growth, differentiation, and hemoglobinization of erythroid primary cells. Endothelial NOS (eNOS) mRNA and protein levels, as well as bioactivity, decrease during erythroid differentiation, concomitantly with the elevation of hemoglobin levels. Human red blood cells (RBCs) have been reported to contain some eNOS activity; NO appears to affect RBC's deformability. Generally, NO activates cellular soluble guanylyl cyclase (sGC) to produce a second messenger molecule cGMP. NO increases cGMP, γ-globin, and HbF levels in human erythroid cells whereas inhibition of sGC prevents NO-induced increase in γ-globin gene expression. Activation of sGC increases γ-globin gene expression in primary human erythroblasts. High cAMP levels continuously decrease in contrast to steady but low levels of cGMP during erythroid differentiation. The activation of the cAMP pathway has also been reported to induce expression of the γ-globin gene in human erythroid cells. NO is hydrophobic and accumulates in lipid membranes, and most autoxidation to nitrite in vivo occurs there. The reaction of NO with deoxyhemoglobin produces nitrosylhemoglobin (HbFe(II)NO), while that with oxyhemoglobin produced methemoglobin and nitrate. Nitrite can also react with deoxyhemoglobin to produce NO. This reaction as well as the postulated formation of a thiol-NO derivative of hemoglobin (SNO-Hb) appears to be major mechanisms for the preservation and transport of NO bioactivity by red cells-making NO act as a "hormone." Thus, RBCs and hemoglobin molecules are essential factors in regulating the bioactivity of NO throughout the mammalian body and may be important in the pathophysiology of several circulatory diseases and be the basis for new therapeutic approaches to these diseases. © 2008 Elsevier Inc. All rights reserved.",
journal = "Current Topics in Developmental Biology",
title = "Effects of Nitric Oxide on Red Blood Cell Development and Phenotype",
pages = "215-169",
volume = "82",
doi = "10.1016/S0070-2153(07)00007-5"
}

Čokić, V.,& Schechter, A. N.. (2008). Effects of Nitric Oxide on Red Blood Cell Development and Phenotype. in Current Topics in Developmental Biology, 82, 169-215.
https://doi.org/10.1016/S0070-2153(07)00007-5

Čokić V, Schechter AN. Effects of Nitric Oxide on Red Blood Cell Development and Phenotype. in Current Topics in Developmental Biology. 2008;82:169-215.
doi:10.1016/S0070-2153(07)00007-5 .

Čokić, Vladan, Schechter, Alan N., "Effects of Nitric Oxide on Red Blood Cell Development and Phenotype" in Current Topics in Developmental Biology, 82 (2008):169-215,
https://doi.org/10.1016/S0070-2153(07)00007-5 . .

TY  - JOUR
AU  - Čokić, Vladan
AU  - Andrić, Silvana A.
AU  - Stojilković, Stanko S.
AU  - Noguchi, Constance T.
AU  - Schechter, Alan N.
PY  - 2008
UR  - http://rimi.imi.bg.ac.rs/handle/123456789/202
AB  - Hydroxyurea, a drug widely used for treating myeloproliferative diseases, has also been approved for the treatment of sickle cell disease by raising fetal hemoglobin (HbF). We have shown that nitric oxide (NO) and the soluble guanylyl cyclase (sGC) pathways are involved in hydroxyurea induction of HbF levels in erythroid progenitor cells (EPCs). We demonstrate now that during erythroid differentiation, endothelial NO synthase mRNA and protein levels decline steadily, as does the production of NO derivatives and cyclic adenosine monophosphate (cAMP) levels, but guanosine 3',5'-cyclic monophosphate (cGMP) levels are stable. Hydroxyurea increased intracellular cGMP levels and cAMP levels in EPCs. The NO donor, DEANONOate, induced much higher cGMP levels, but reduced cAMP levels. Hydroxyurea (1 mM) induced production of approximately 45 pM cGMP/minute/ng of purified sGC, similar to induction by 1 mu M DEANONOate. We found that hydroxyurea and ProliNONOate produced iron-nitrosyl derivatives of sGC. Thus, we confirm that hydroxyurea can directly interact with the deoxy-heme of sGC, presumably by a free-radical nitroxide pathway, and activate cGMP production. These data add to an expanding appreciation of the role of hydroxyurea as an inducer of the NO/cGMP pathway in EPCs. These mechanisms may also be involved in the cytostatic effects of hydroxyurea, as well as the induction of HbF.
PB  - Amer Soc Hematology, Washington
T2  - Blood
T1  - Hydroxyurea nitrosylates and activates soluble guanylyl cyclase in human erythroid cells
EP  - 1123
IS  - 3
SP  - 1117
VL  - 111
DO  - 10.1182/blood-2007-05-088732
ER  - 

@article{
author = "Čokić, Vladan and Andrić, Silvana A. and Stojilković, Stanko S. and Noguchi, Constance T. and Schechter, Alan N.",
year = "2008",
abstract = "Hydroxyurea, a drug widely used for treating myeloproliferative diseases, has also been approved for the treatment of sickle cell disease by raising fetal hemoglobin (HbF). We have shown that nitric oxide (NO) and the soluble guanylyl cyclase (sGC) pathways are involved in hydroxyurea induction of HbF levels in erythroid progenitor cells (EPCs). We demonstrate now that during erythroid differentiation, endothelial NO synthase mRNA and protein levels decline steadily, as does the production of NO derivatives and cyclic adenosine monophosphate (cAMP) levels, but guanosine 3',5'-cyclic monophosphate (cGMP) levels are stable. Hydroxyurea increased intracellular cGMP levels and cAMP levels in EPCs. The NO donor, DEANONOate, induced much higher cGMP levels, but reduced cAMP levels. Hydroxyurea (1 mM) induced production of approximately 45 pM cGMP/minute/ng of purified sGC, similar to induction by 1 mu M DEANONOate. We found that hydroxyurea and ProliNONOate produced iron-nitrosyl derivatives of sGC. Thus, we confirm that hydroxyurea can directly interact with the deoxy-heme of sGC, presumably by a free-radical nitroxide pathway, and activate cGMP production. These data add to an expanding appreciation of the role of hydroxyurea as an inducer of the NO/cGMP pathway in EPCs. These mechanisms may also be involved in the cytostatic effects of hydroxyurea, as well as the induction of HbF.",
publisher = "Amer Soc Hematology, Washington",
journal = "Blood",
title = "Hydroxyurea nitrosylates and activates soluble guanylyl cyclase in human erythroid cells",
pages = "1123-1117",
number = "3",
volume = "111",
doi = "10.1182/blood-2007-05-088732"
}

Čokić, V., Andrić, S. A., Stojilković, S. S., Noguchi, C. T.,& Schechter, A. N.. (2008). Hydroxyurea nitrosylates and activates soluble guanylyl cyclase in human erythroid cells. in Blood
Amer Soc Hematology, Washington., 111(3), 1117-1123.
https://doi.org/10.1182/blood-2007-05-088732

Čokić V, Andrić SA, Stojilković SS, Noguchi CT, Schechter AN. Hydroxyurea nitrosylates and activates soluble guanylyl cyclase in human erythroid cells. in Blood. 2008;111(3):1117-1123.
doi:10.1182/blood-2007-05-088732 .

Čokić, Vladan, Andrić, Silvana A., Stojilković, Stanko S., Noguchi, Constance T., Schechter, Alan N., "Hydroxyurea nitrosylates and activates soluble guanylyl cyclase in human erythroid cells" in Blood, 111, no. 3 (2008):1117-1123,
https://doi.org/10.1182/blood-2007-05-088732 . .

TY  - JOUR
AU  - Čokić, Vladan
AU  - Beleslin-Čokić, Bojana
AU  - Noguchi, Constance T.
AU  - Schechter, Alan N.
PY  - 2007
UR  - http://rimi.imi.bg.ac.rs/handle/123456789/174
AB  - Recent reports have identified the proteasome as the primary degradation pathway for inducible, neuronal and endothelial nitric oxide synthase (NOS). We have demonstrated that hydroxyurea increased nitric oxide (NO) production in endothelial cells through phosphorylation of eNOS as a short-term effect. We find now that NO production in endothelial cells is dose-dependently stimulated by hydroxyurea, as well as both specific and non-specific proteasome inhibitors, as a long term effect. Prolonged treatment of primary human umbilical vein endothelial cells (HUVEC) with hydroxyurea was found to increase eNOS protein levels without an effect on eNOS mRNA levels, suggesting posttranscriptional control. We observed that the inhibitors of proteasomes that we tested also increased eNOS protein levels in HUVEC. In a proteasome assay, we showed that hydroxyurea inhibited protein degradation in a dose-dependent manner, in both purified 20S proteasome and HUVEC lysates. The NO production induced by hydroxyurea in endothelial cells appears to be mediated by long term posttranscriptional augmentation in eNOS levels via inhibition of the proteasome activity. Published by Elsevier Inc.
PB  - Academic Press Inc Elsevier Science, San Diego
T2  - Nitric Oxide-Biology & Chemistry
T1  - Hydroxyurea increases eNOS protein levels through inhibition of proteasome activity
EP  - 378
IS  - 3
SP  - 371
VL  - 16
DO  - 10.1016/j.niox.2007.01.001
ER  - 

@article{
author = "Čokić, Vladan and Beleslin-Čokić, Bojana and Noguchi, Constance T. and Schechter, Alan N.",
year = "2007",
abstract = "Recent reports have identified the proteasome as the primary degradation pathway for inducible, neuronal and endothelial nitric oxide synthase (NOS). We have demonstrated that hydroxyurea increased nitric oxide (NO) production in endothelial cells through phosphorylation of eNOS as a short-term effect. We find now that NO production in endothelial cells is dose-dependently stimulated by hydroxyurea, as well as both specific and non-specific proteasome inhibitors, as a long term effect. Prolonged treatment of primary human umbilical vein endothelial cells (HUVEC) with hydroxyurea was found to increase eNOS protein levels without an effect on eNOS mRNA levels, suggesting posttranscriptional control. We observed that the inhibitors of proteasomes that we tested also increased eNOS protein levels in HUVEC. In a proteasome assay, we showed that hydroxyurea inhibited protein degradation in a dose-dependent manner, in both purified 20S proteasome and HUVEC lysates. The NO production induced by hydroxyurea in endothelial cells appears to be mediated by long term posttranscriptional augmentation in eNOS levels via inhibition of the proteasome activity. Published by Elsevier Inc.",
publisher = "Academic Press Inc Elsevier Science, San Diego",
journal = "Nitric Oxide-Biology & Chemistry",
title = "Hydroxyurea increases eNOS protein levels through inhibition of proteasome activity",
pages = "378-371",
number = "3",
volume = "16",
doi = "10.1016/j.niox.2007.01.001"
}

Čokić, V., Beleslin-Čokić, B., Noguchi, C. T.,& Schechter, A. N.. (2007). Hydroxyurea increases eNOS protein levels through inhibition of proteasome activity. in Nitric Oxide-Biology & Chemistry
Academic Press Inc Elsevier Science, San Diego., 16(3), 371-378.
https://doi.org/10.1016/j.niox.2007.01.001

Čokić V, Beleslin-Čokić B, Noguchi CT, Schechter AN. Hydroxyurea increases eNOS protein levels through inhibition of proteasome activity. in Nitric Oxide-Biology & Chemistry. 2007;16(3):371-378.
doi:10.1016/j.niox.2007.01.001 .

Čokić, Vladan, Beleslin-Čokić, Bojana, Noguchi, Constance T., Schechter, Alan N., "Hydroxyurea increases eNOS protein levels through inhibition of proteasome activity" in Nitric Oxide-Biology & Chemistry, 16, no. 3 (2007):371-378,
https://doi.org/10.1016/j.niox.2007.01.001 . .

TY  - CONF
AU  - Čokić, Vladan
AU  - Bhattacharya, Bhaskar
AU  - Smith, Reginald D.
AU  - Beleslin-Čokić, Bojana
AU  - Noguchi, Constance T.
AU  - Puri, Raj K.
AU  - Schechter, Alan N.
PY  - 2007
UR  - http://rimi.imi.bg.ac.rs/handle/123456789/177
PB  - Academic Press Inc Elsevier Science, San Diego
C3  - Blood Cells Molecules & Diseases
T1  - Gene expression profiling in fetal and adult definitive erythropoiesis
EP  - 132
IS  - 2
SP  - 131
VL  - 38
DO  - 10.1016/j.bcmd.2006.10.031
ER  - 

@conference{
author = "Čokić, Vladan and Bhattacharya, Bhaskar and Smith, Reginald D. and Beleslin-Čokić, Bojana and Noguchi, Constance T. and Puri, Raj K. and Schechter, Alan N.",
year = "2007",
publisher = "Academic Press Inc Elsevier Science, San Diego",
journal = "Blood Cells Molecules & Diseases",
title = "Gene expression profiling in fetal and adult definitive erythropoiesis",
pages = "132-131",
number = "2",
volume = "38",
doi = "10.1016/j.bcmd.2006.10.031"
}

Čokić, V., Bhattacharya, B., Smith, R. D., Beleslin-Čokić, B., Noguchi, C. T., Puri, R. K.,& Schechter, A. N.. (2007). Gene expression profiling in fetal and adult definitive erythropoiesis. in Blood Cells Molecules & Diseases
Academic Press Inc Elsevier Science, San Diego., 38(2), 131-132.
https://doi.org/10.1016/j.bcmd.2006.10.031

Čokić V, Bhattacharya B, Smith RD, Beleslin-Čokić B, Noguchi CT, Puri RK, Schechter AN. Gene expression profiling in fetal and adult definitive erythropoiesis. in Blood Cells Molecules & Diseases. 2007;38(2):131-132.
doi:10.1016/j.bcmd.2006.10.031 .

Čokić, Vladan, Bhattacharya, Bhaskar, Smith, Reginald D., Beleslin-Čokić, Bojana, Noguchi, Constance T., Puri, Raj K., Schechter, Alan N., "Gene expression profiling in fetal and adult definitive erythropoiesis" in Blood Cells Molecules & Diseases, 38, no. 2 (2007):131-132,
https://doi.org/10.1016/j.bcmd.2006.10.031 . .

TY  - CONF
AU  - Čokić, Vladan
AU  - Beleslin-Čokić, Bojana
AU  - Noguchi, Constance T.
AU  - Schechter, Alan N.
PY  - 2007
UR  - http://rimi.imi.bg.ac.rs/handle/123456789/167
PB  - Amer Soc Hematology, Washington
C3  - Blood
T1  - Globin genes induction by nitric oxide of stromal cell origin
EP  - 94B
IS  - 11
SP  - 94B
VL  - 110
DO  - 10.1182/blood.V110.11.4102.4102
ER  - 

@conference{
author = "Čokić, Vladan and Beleslin-Čokić, Bojana and Noguchi, Constance T. and Schechter, Alan N.",
year = "2007",
publisher = "Amer Soc Hematology, Washington",
journal = "Blood",
title = "Globin genes induction by nitric oxide of stromal cell origin",
pages = "94B-94B",
number = "11",
volume = "110",
doi = "10.1182/blood.V110.11.4102.4102"
}

Čokić, V., Beleslin-Čokić, B., Noguchi, C. T.,& Schechter, A. N.. (2007). Globin genes induction by nitric oxide of stromal cell origin. in Blood
Amer Soc Hematology, Washington., 110(11), 94B-94B.
https://doi.org/10.1182/blood.V110.11.4102.4102

Čokić V, Beleslin-Čokić B, Noguchi CT, Schechter AN. Globin genes induction by nitric oxide of stromal cell origin. in Blood. 2007;110(11):94B-94B.
doi:10.1182/blood.V110.11.4102.4102 .

Čokić, Vladan, Beleslin-Čokić, Bojana, Noguchi, Constance T., Schechter, Alan N., "Globin genes induction by nitric oxide of stromal cell origin" in Blood, 110, no. 11 (2007):94B-94B,
https://doi.org/10.1182/blood.V110.11.4102.4102 . .

TY  - CONF
AU  - Čokić, Vladan
AU  - Beleslin-Čokić, Bojana
AU  - Noguchi, Constance T.
AU  - Schechter, Alan N.
PY  - 2007
UR  - http://rimi.imi.bg.ac.rs/handle/123456789/164
PB  - Elsevier Science Inc, New York
C3  - Experimental Hematology
T1  - Hydroxyurea nitrosylates and activates soluble guanylyl cyclase in human erythroid cells
EP  - 106
IS  - 9
SP  - 106
VL  - 35
UR  - https://hdl.handle.net/21.15107/rcub_rimi_164
ER  - 

@conference{
author = "Čokić, Vladan and Beleslin-Čokić, Bojana and Noguchi, Constance T. and Schechter, Alan N.",
year = "2007",
publisher = "Elsevier Science Inc, New York",
journal = "Experimental Hematology",
title = "Hydroxyurea nitrosylates and activates soluble guanylyl cyclase in human erythroid cells",
pages = "106-106",
number = "9",
volume = "35",
url = "https://hdl.handle.net/21.15107/rcub_rimi_164"
}

Čokić, V., Beleslin-Čokić, B., Noguchi, C. T.,& Schechter, A. N.. (2007). Hydroxyurea nitrosylates and activates soluble guanylyl cyclase in human erythroid cells. in Experimental Hematology
Elsevier Science Inc, New York., 35(9), 106-106.
https://hdl.handle.net/21.15107/rcub_rimi_164

Čokić V, Beleslin-Čokić B, Noguchi CT, Schechter AN. Hydroxyurea nitrosylates and activates soluble guanylyl cyclase in human erythroid cells. in Experimental Hematology. 2007;35(9):106-106.
https://hdl.handle.net/21.15107/rcub_rimi_164 .

Čokić, Vladan, Beleslin-Čokić, Bojana, Noguchi, Constance T., Schechter, Alan N., "Hydroxyurea nitrosylates and activates soluble guanylyl cyclase in human erythroid cells" in Experimental Hematology, 35, no. 9 (2007):106-106,
https://hdl.handle.net/21.15107/rcub_rimi_164 .

TY  - JOUR
AU  - Čokić, Vladan
AU  - Beleslin-Čokić, Bojana
AU  - Tomić, Melanija
AU  - Stojilković, Stanko S.
AU  - Noguchi, Constance T.
AU  - Schechter, Alan N.
PY  - 2006
UR  - http://rimi.imi.bg.ac.rs/handle/123456789/150
AB  - Hydroxyurea is a cell-cycle-specific drug that has been used to treat myeloproliferative diseases and sickle cell anemia. We have recently shown that hydroxyurea, like nitric oxide (NO)-donor compounds, increased cGMP levels in human erythroid cells. We show now that hydroxyurea increases endothelial-cell production of NO; this induction of NO in human umbilical vein endothelial cells (HUVECs) and human bone marrow endothelial cell line (TrHBMEC) is blocked by competitive inhibitors of NO synthase (NOS), such as N-G-nitro-L-arginine-methyl ester (L-NAME) and N-G-nitro-L-arginine. It is dependent on cAMP-dependent protein kinase (PKA) and protein kinase B (PKB/Akt) activity. We found that hydroxyurea dose- and time-dependently induced rapid and transient phosphorylation of eNOS at Ser1177 in a PKA-dependent manner; inhibitors of PKB/Akt could partially abrogate this effect. In addition, hydroxyurea induced cAMP and cGMP levels in a dose-dependent manner, as well as levels of intracellular calcium in HUVECs. These studies established an additional mechanism by which rapid and sustained effects of hydroxyurea may affect cellular NO levels and perhaps enhance the effect of NO in myeloproliferative diseases.
PB  - Amer Soc Hematology, Washington
T2  - Blood
T1  - Hydroxyurea induces the eNOS-cGMP pathway in endothelial cells
EP  - 191
IS  - 1
SP  - 184
VL  - 108
DO  - 10.1182/blood-2005-11-4454
ER  - 

@article{
author = "Čokić, Vladan and Beleslin-Čokić, Bojana and Tomić, Melanija and Stojilković, Stanko S. and Noguchi, Constance T. and Schechter, Alan N.",
year = "2006",
abstract = "Hydroxyurea is a cell-cycle-specific drug that has been used to treat myeloproliferative diseases and sickle cell anemia. We have recently shown that hydroxyurea, like nitric oxide (NO)-donor compounds, increased cGMP levels in human erythroid cells. We show now that hydroxyurea increases endothelial-cell production of NO; this induction of NO in human umbilical vein endothelial cells (HUVECs) and human bone marrow endothelial cell line (TrHBMEC) is blocked by competitive inhibitors of NO synthase (NOS), such as N-G-nitro-L-arginine-methyl ester (L-NAME) and N-G-nitro-L-arginine. It is dependent on cAMP-dependent protein kinase (PKA) and protein kinase B (PKB/Akt) activity. We found that hydroxyurea dose- and time-dependently induced rapid and transient phosphorylation of eNOS at Ser1177 in a PKA-dependent manner; inhibitors of PKB/Akt could partially abrogate this effect. In addition, hydroxyurea induced cAMP and cGMP levels in a dose-dependent manner, as well as levels of intracellular calcium in HUVECs. These studies established an additional mechanism by which rapid and sustained effects of hydroxyurea may affect cellular NO levels and perhaps enhance the effect of NO in myeloproliferative diseases.",
publisher = "Amer Soc Hematology, Washington",
journal = "Blood",
title = "Hydroxyurea induces the eNOS-cGMP pathway in endothelial cells",
pages = "191-184",
number = "1",
volume = "108",
doi = "10.1182/blood-2005-11-4454"
}

Čokić, V., Beleslin-Čokić, B., Tomić, M., Stojilković, S. S., Noguchi, C. T.,& Schechter, A. N.. (2006). Hydroxyurea induces the eNOS-cGMP pathway in endothelial cells. in Blood
Amer Soc Hematology, Washington., 108(1), 184-191.
https://doi.org/10.1182/blood-2005-11-4454

Čokić V, Beleslin-Čokić B, Tomić M, Stojilković SS, Noguchi CT, Schechter AN. Hydroxyurea induces the eNOS-cGMP pathway in endothelial cells. in Blood. 2006;108(1):184-191.
doi:10.1182/blood-2005-11-4454 .

Čokić, Vladan, Beleslin-Čokić, Bojana, Tomić, Melanija, Stojilković, Stanko S., Noguchi, Constance T., Schechter, Alan N., "Hydroxyurea induces the eNOS-cGMP pathway in endothelial cells" in Blood, 108, no. 1 (2006):184-191,
https://doi.org/10.1182/blood-2005-11-4454 . .

TY  - CONF
AU  - Čokić, Vladan
AU  - Economou, AP
AU  - Wahl, LM
AU  - Milenković, P.
AU  - Schechter, Alan N.
PY  - 2005
UR  - http://rimi.imi.bg.ac.rs/handle/123456789/125
PB  - Elsevier Science Inc, New York
C3  - Experimental Hematology
T1  - G protein-coupled receptors in hydroxyurea activation of nitric oxide/CGMP pathways and gamma-globin induction
EP  - 80
IS  - 7
SP  - 80
VL  - 33
UR  - https://hdl.handle.net/21.15107/rcub_rimi_125
ER  - 

@conference{
author = "Čokić, Vladan and Economou, AP and Wahl, LM and Milenković, P. and Schechter, Alan N.",
year = "2005",
publisher = "Elsevier Science Inc, New York",
journal = "Experimental Hematology",
title = "G protein-coupled receptors in hydroxyurea activation of nitric oxide/CGMP pathways and gamma-globin induction",
pages = "80-80",
number = "7",
volume = "33",
url = "https://hdl.handle.net/21.15107/rcub_rimi_125"
}

Čokić, V., Economou, A., Wahl, L., Milenković, P.,& Schechter, A. N.. (2005). G protein-coupled receptors in hydroxyurea activation of nitric oxide/CGMP pathways and gamma-globin induction. in Experimental Hematology
Elsevier Science Inc, New York., 33(7), 80-80.
https://hdl.handle.net/21.15107/rcub_rimi_125

Čokić V, Economou A, Wahl L, Milenković P, Schechter AN. G protein-coupled receptors in hydroxyurea activation of nitric oxide/CGMP pathways and gamma-globin induction. in Experimental Hematology. 2005;33(7):80-80.
https://hdl.handle.net/21.15107/rcub_rimi_125 .

Čokić, Vladan, Economou, AP, Wahl, LM, Milenković, P., Schechter, Alan N., "G protein-coupled receptors in hydroxyurea activation of nitric oxide/CGMP pathways and gamma-globin induction" in Experimental Hematology, 33, no. 7 (2005):80-80,
https://hdl.handle.net/21.15107/rcub_rimi_125 .

TY  - CONF
AU  - Čokić, Vladan
AU  - Beleslin-Čokić, Bojana
AU  - Noguchi, Constance T.
AU  - Schechter, Alan N.
PY  - 2005
UR  - http://rimi.imi.bg.ac.rs/handle/123456789/126
PB  - Elsevier Science Inc, New York
C3  - Experimental Hematology
T1  - Hydroxyurea induces eNOS activity and protein levels in endothelial cells
EP  - 88
IS  - 7
SP  - 87
VL  - 33
UR  - https://hdl.handle.net/21.15107/rcub_rimi_126
ER  - 

@conference{
author = "Čokić, Vladan and Beleslin-Čokić, Bojana and Noguchi, Constance T. and Schechter, Alan N.",
year = "2005",
publisher = "Elsevier Science Inc, New York",
journal = "Experimental Hematology",
title = "Hydroxyurea induces eNOS activity and protein levels in endothelial cells",
pages = "88-87",
number = "7",
volume = "33",
url = "https://hdl.handle.net/21.15107/rcub_rimi_126"
}

Čokić, V., Beleslin-Čokić, B., Noguchi, C. T.,& Schechter, A. N.. (2005). Hydroxyurea induces eNOS activity and protein levels in endothelial cells. in Experimental Hematology
Elsevier Science Inc, New York., 33(7), 87-88.
https://hdl.handle.net/21.15107/rcub_rimi_126

Čokić V, Beleslin-Čokić B, Noguchi CT, Schechter AN. Hydroxyurea induces eNOS activity and protein levels in endothelial cells. in Experimental Hematology. 2005;33(7):87-88.
https://hdl.handle.net/21.15107/rcub_rimi_126 .

Čokić, Vladan, Beleslin-Čokić, Bojana, Noguchi, Constance T., Schechter, Alan N., "Hydroxyurea induces eNOS activity and protein levels in endothelial cells" in Experimental Hematology, 33, no. 7 (2005):87-88,
https://hdl.handle.net/21.15107/rcub_rimi_126 .