RIMI - Repository of the Institute for Medical Research
Institute for Medical Research
    • English
    • Српски
    • Српски (Serbia)
  • English 
    • English
    • Serbian (Cyrillic)
    • Serbian (Latin)
  • Login
View Item 
  •   RIMI
  • Institut za medicinska istraživanja
  • Radovi istraživača / Researchers' publications
  • View Item
  •   RIMI
  • Institut za medicinska istraživanja
  • Radovi istraživača / Researchers' publications
  • View Item
JavaScript is disabled for your browser. Some features of this site may not work without it.

Urokinase type plasminogen activator mediates Interleukin-17-induced peripheral blood mesenchymal stem cell motility and transendothelial migration

Thumbnail
2015
663.pdf (1.824Mb)
Authors
Krstić, Jelena
Obradović, Hristina
Jauković, Aleksandra
Okić-Đorđević, Ivana
Trivanović, Drenka
Kukolj, Tamara
Mojsilović, Slavko
Ilić, Vesna
Santibanez, Juan
Bugarski, Diana
Article (Published version)
Metadata
Show full item record
Abstract
Mesenchymal stem cells (MSCs) have the potential to migrate toward damaged tissues increasing tissue regeneration. Interleukin-17 (IL-17) is a proinflammatory cytokine with pleiotropic effects associated with many inflammatory diseases. Although IL-17 can modulate MSC functions, its capacity to regulate MSC migration is not well elucidated so far. Here, we studied the role of IL-17 on peripheral blood (PB) derived MSC migration and transmigration across endothelial cells. IL-17 increased PB-MSC migration in a wound healing assay as well as cell mobilization from collagen gel. Concomitantly IL-17 induced the expression of urokinase type plasminogen activator (uPA) without affecting matrix metalloproteinase expression. The incremented uPA expression mediated the capacity of IL-17 to enhance PB-MSC migration in a ERK1,2 MAPK dependent way. Also, IL-17 induced PB-MSC migration alongside with changes in cell polarization and uPA localization in cell protrusions. Moreover, IL-17 increased PB...-MSC adhesion to endothelial cells and transendothelial migration, as well as increased the capacity of PB-MSC adhesion to fibronectin, in an uPA-dependent fashion. Therefore, our data suggested that IL-17 may act as chemotropic factor for PB-MSCs by incrementing cell motility and uPA expression during inflammation development.

Keywords:
Interleukin-17 / Peripheral blood mesenchymal stem cells / Urokinase type plasminogen activator / Migration / Transendothelial migration
Source:
Biochimica et Biophysica Acta-Molecular Cell Research, 2015, 1853, 2, 431-444
Publisher:
  • Elsevier Science Bv, Amsterdam
Funding / projects:
  • Regenerative and modulatory potential of adult stem cells (RS-175062)

DOI: 10.1016/j.bbamcr.2014.11.025

ISSN: 0167-4889

PubMed: 25433194

WoS: 000348554600017

Scopus: 2-s2.0-84916910734
[ Google Scholar ]
28
24
URI
http://rimi.imi.bg.ac.rs/handle/123456789/666
Collections
  • Radovi istraživača / Researchers' publications
Institution/Community
Institut za medicinska istraživanja
TY  - JOUR
AU  - Krstić, Jelena
AU  - Obradović, Hristina
AU  - Jauković, Aleksandra
AU  - Okić-Đorđević, Ivana
AU  - Trivanović, Drenka
AU  - Kukolj, Tamara
AU  - Mojsilović, Slavko
AU  - Ilić, Vesna
AU  - Santibanez, Juan
AU  - Bugarski, Diana
PY  - 2015
UR  - http://rimi.imi.bg.ac.rs/handle/123456789/666
AB  - Mesenchymal stem cells (MSCs) have the potential to migrate toward damaged tissues increasing tissue regeneration. Interleukin-17 (IL-17) is a proinflammatory cytokine with pleiotropic effects associated with many inflammatory diseases. Although IL-17 can modulate MSC functions, its capacity to regulate MSC migration is not well elucidated so far. Here, we studied the role of IL-17 on peripheral blood (PB) derived MSC migration and transmigration across endothelial cells. IL-17 increased PB-MSC migration in a wound healing assay as well as cell mobilization from collagen gel. Concomitantly IL-17 induced the expression of urokinase type plasminogen activator (uPA) without affecting matrix metalloproteinase expression. The incremented uPA expression mediated the capacity of IL-17 to enhance PB-MSC migration in a ERK1,2 MAPK dependent way. Also, IL-17 induced PB-MSC migration alongside with changes in cell polarization and uPA localization in cell protrusions. Moreover, IL-17 increased PB-MSC adhesion to endothelial cells and transendothelial migration, as well as increased the capacity of PB-MSC adhesion to fibronectin, in an uPA-dependent fashion. Therefore, our data suggested that IL-17 may act as chemotropic factor for PB-MSCs by incrementing cell motility and uPA expression during inflammation development.
PB  - Elsevier Science Bv, Amsterdam
T2  - Biochimica et Biophysica Acta-Molecular Cell Research
T1  - Urokinase type plasminogen activator mediates Interleukin-17-induced peripheral blood mesenchymal stem cell motility and transendothelial migration
EP  - 444
IS  - 2
SP  - 431
VL  - 1853
DO  - 10.1016/j.bbamcr.2014.11.025
ER  - 
@article{
author = "Krstić, Jelena and Obradović, Hristina and Jauković, Aleksandra and Okić-Đorđević, Ivana and Trivanović, Drenka and Kukolj, Tamara and Mojsilović, Slavko and Ilić, Vesna and Santibanez, Juan and Bugarski, Diana",
year = "2015",
abstract = "Mesenchymal stem cells (MSCs) have the potential to migrate toward damaged tissues increasing tissue regeneration. Interleukin-17 (IL-17) is a proinflammatory cytokine with pleiotropic effects associated with many inflammatory diseases. Although IL-17 can modulate MSC functions, its capacity to regulate MSC migration is not well elucidated so far. Here, we studied the role of IL-17 on peripheral blood (PB) derived MSC migration and transmigration across endothelial cells. IL-17 increased PB-MSC migration in a wound healing assay as well as cell mobilization from collagen gel. Concomitantly IL-17 induced the expression of urokinase type plasminogen activator (uPA) without affecting matrix metalloproteinase expression. The incremented uPA expression mediated the capacity of IL-17 to enhance PB-MSC migration in a ERK1,2 MAPK dependent way. Also, IL-17 induced PB-MSC migration alongside with changes in cell polarization and uPA localization in cell protrusions. Moreover, IL-17 increased PB-MSC adhesion to endothelial cells and transendothelial migration, as well as increased the capacity of PB-MSC adhesion to fibronectin, in an uPA-dependent fashion. Therefore, our data suggested that IL-17 may act as chemotropic factor for PB-MSCs by incrementing cell motility and uPA expression during inflammation development.",
publisher = "Elsevier Science Bv, Amsterdam",
journal = "Biochimica et Biophysica Acta-Molecular Cell Research",
title = "Urokinase type plasminogen activator mediates Interleukin-17-induced peripheral blood mesenchymal stem cell motility and transendothelial migration",
pages = "444-431",
number = "2",
volume = "1853",
doi = "10.1016/j.bbamcr.2014.11.025"
}
Krstić, J., Obradović, H., Jauković, A., Okić-Đorđević, I., Trivanović, D., Kukolj, T., Mojsilović, S., Ilić, V., Santibanez, J.,& Bugarski, D.. (2015). Urokinase type plasminogen activator mediates Interleukin-17-induced peripheral blood mesenchymal stem cell motility and transendothelial migration. in Biochimica et Biophysica Acta-Molecular Cell Research
Elsevier Science Bv, Amsterdam., 1853(2), 431-444.
https://doi.org/10.1016/j.bbamcr.2014.11.025
conv_3428
Krstić J, Obradović H, Jauković A, Okić-Đorđević I, Trivanović D, Kukolj T, Mojsilović S, Ilić V, Santibanez J, Bugarski D. Urokinase type plasminogen activator mediates Interleukin-17-induced peripheral blood mesenchymal stem cell motility and transendothelial migration. in Biochimica et Biophysica Acta-Molecular Cell Research. 2015;1853(2):431-444.
doi:10.1016/j.bbamcr.2014.11.025
conv_3428 .
Krstić, Jelena, Obradović, Hristina, Jauković, Aleksandra, Okić-Đorđević, Ivana, Trivanović, Drenka, Kukolj, Tamara, Mojsilović, Slavko, Ilić, Vesna, Santibanez, Juan, Bugarski, Diana, "Urokinase type plasminogen activator mediates Interleukin-17-induced peripheral blood mesenchymal stem cell motility and transendothelial migration" in Biochimica et Biophysica Acta-Molecular Cell Research, 1853, no. 2 (2015):431-444,
https://doi.org/10.1016/j.bbamcr.2014.11.025 .,
conv_3428 .

DSpace software copyright © 2002-2015  DuraSpace
About RIMI | Send Feedback

OpenAIRERCUB
 

 

All of DSpaceCommunitiesAuthorsTitlesSubjectsThis institutionAuthorsTitlesSubjects

Statistics

View Usage Statistics

DSpace software copyright © 2002-2015  DuraSpace
About RIMI | Send Feedback

OpenAIRERCUB