Interleukin-17 modulates myoblast cell migration by inhibiting urokinase type plasminogen activator expression through p38 mitogen-activated protein kinase
Само за регистроване кориснике
2013
Аутори
Krstić, JelenaSantibanez, Juan F.
Krstić, Aleksandra
Mojsilović, Slavko
Ilić, Vesna
Bugarski, Diana
Чланак у часопису (Објављена верзија)
Метаподаци
Приказ свих података о документуАпстракт
Interleukin-17 belongs to a family of pro-inflammatory cytokines with pleiotropic effects, which can be associated with several inflammatory diseases of the muscle tissue. Although elevated levels of interleukin-17 have been described in inflammatory myopathies, its role in muscle homeostasis remains to be elucidated. The requirement of the urokinase type plasminogen activator in skeletal myogenesis was recently demonstrated in vivo and in vitro, suggesting its involvement in the regulation of extracellular matrix remodeling, cell migration and myoblast fusion. Our previous results have demonstrated that interleukin-17 inhibits myogenic differentiation of C2C12 myoblasts in vitro concomitantly with the inhibition of cell migration. However, the involvement of urokinase type plasminogen activator in interleukin-17-inhibited myogenesis and migration remained to be analyzed. Therefore, the effect of interleukin-17 on the production of urokinase type plasminogen activator by C2C12 myoblast...s was determined in the present study. Our results demonstrated that interleukin-17 strongly inhibits urokinase type plasminogen activator expression during myogenic differentiation. This reduction of urokinase type plasminogen activator production corresponded with the inhibition of cell migration by interleukin-17. Activation of p38 signaling pathway elicited by interleukin-17 mediated the inhibition of both urokinase type plasminogen activator expression and cell migration. Additionally, IL-17 inhibited C2C12 cells migration by causing the cells to reorganize their cytoskeleton and lose polarity. Therefore, our results suggest a novel mechanism by which interleukin-17 regulates myogenic differentiation through the inhibition of urokinase type plasminogen activator expression and cell migration. Accordingly, interleukin-17 may represent a potential clinical target worth investigating for the treatment of inflammatory, muscle diseases.
Кључне речи:
Myoblast / IL-17 / p38 / uPA / Migration / DifferentiationИзвор:
International Journal of Biochemistry & Cell Biology, 2013, 45, 2, 464-475Издавач:
- Pergamon-Elsevier Science Ltd, Oxford
Финансирање / пројекти:
- Регенеративни и модулаторни потенцијал адултних матичних ћелија (RS-MESTD-Basic Research (BR or ON)-175062)
DOI: 10.1016/j.biocel.2012.11.010
ISSN: 1357-2725
PubMed: 23183001
WoS: 000315251500030
Scopus: 2-s2.0-84872290003
Институција/група
Institut za medicinska istraživanjaTY - JOUR AU - Krstić, Jelena AU - Santibanez, Juan F. AU - Krstić, Aleksandra AU - Mojsilović, Slavko AU - Ilić, Vesna AU - Bugarski, Diana PY - 2013 UR - http://rimi.imi.bg.ac.rs/handle/123456789/514 AB - Interleukin-17 belongs to a family of pro-inflammatory cytokines with pleiotropic effects, which can be associated with several inflammatory diseases of the muscle tissue. Although elevated levels of interleukin-17 have been described in inflammatory myopathies, its role in muscle homeostasis remains to be elucidated. The requirement of the urokinase type plasminogen activator in skeletal myogenesis was recently demonstrated in vivo and in vitro, suggesting its involvement in the regulation of extracellular matrix remodeling, cell migration and myoblast fusion. Our previous results have demonstrated that interleukin-17 inhibits myogenic differentiation of C2C12 myoblasts in vitro concomitantly with the inhibition of cell migration. However, the involvement of urokinase type plasminogen activator in interleukin-17-inhibited myogenesis and migration remained to be analyzed. Therefore, the effect of interleukin-17 on the production of urokinase type plasminogen activator by C2C12 myoblasts was determined in the present study. Our results demonstrated that interleukin-17 strongly inhibits urokinase type plasminogen activator expression during myogenic differentiation. This reduction of urokinase type plasminogen activator production corresponded with the inhibition of cell migration by interleukin-17. Activation of p38 signaling pathway elicited by interleukin-17 mediated the inhibition of both urokinase type plasminogen activator expression and cell migration. Additionally, IL-17 inhibited C2C12 cells migration by causing the cells to reorganize their cytoskeleton and lose polarity. Therefore, our results suggest a novel mechanism by which interleukin-17 regulates myogenic differentiation through the inhibition of urokinase type plasminogen activator expression and cell migration. Accordingly, interleukin-17 may represent a potential clinical target worth investigating for the treatment of inflammatory, muscle diseases. PB - Pergamon-Elsevier Science Ltd, Oxford T2 - International Journal of Biochemistry & Cell Biology T1 - Interleukin-17 modulates myoblast cell migration by inhibiting urokinase type plasminogen activator expression through p38 mitogen-activated protein kinase EP - 475 IS - 2 SP - 464 VL - 45 DO - 10.1016/j.biocel.2012.11.010 ER -
@article{ author = "Krstić, Jelena and Santibanez, Juan F. and Krstić, Aleksandra and Mojsilović, Slavko and Ilić, Vesna and Bugarski, Diana", year = "2013", abstract = "Interleukin-17 belongs to a family of pro-inflammatory cytokines with pleiotropic effects, which can be associated with several inflammatory diseases of the muscle tissue. Although elevated levels of interleukin-17 have been described in inflammatory myopathies, its role in muscle homeostasis remains to be elucidated. The requirement of the urokinase type plasminogen activator in skeletal myogenesis was recently demonstrated in vivo and in vitro, suggesting its involvement in the regulation of extracellular matrix remodeling, cell migration and myoblast fusion. Our previous results have demonstrated that interleukin-17 inhibits myogenic differentiation of C2C12 myoblasts in vitro concomitantly with the inhibition of cell migration. However, the involvement of urokinase type plasminogen activator in interleukin-17-inhibited myogenesis and migration remained to be analyzed. Therefore, the effect of interleukin-17 on the production of urokinase type plasminogen activator by C2C12 myoblasts was determined in the present study. Our results demonstrated that interleukin-17 strongly inhibits urokinase type plasminogen activator expression during myogenic differentiation. This reduction of urokinase type plasminogen activator production corresponded with the inhibition of cell migration by interleukin-17. Activation of p38 signaling pathway elicited by interleukin-17 mediated the inhibition of both urokinase type plasminogen activator expression and cell migration. Additionally, IL-17 inhibited C2C12 cells migration by causing the cells to reorganize their cytoskeleton and lose polarity. Therefore, our results suggest a novel mechanism by which interleukin-17 regulates myogenic differentiation through the inhibition of urokinase type plasminogen activator expression and cell migration. Accordingly, interleukin-17 may represent a potential clinical target worth investigating for the treatment of inflammatory, muscle diseases.", publisher = "Pergamon-Elsevier Science Ltd, Oxford", journal = "International Journal of Biochemistry & Cell Biology", title = "Interleukin-17 modulates myoblast cell migration by inhibiting urokinase type plasminogen activator expression through p38 mitogen-activated protein kinase", pages = "475-464", number = "2", volume = "45", doi = "10.1016/j.biocel.2012.11.010" }
Krstić, J., Santibanez, J. F., Krstić, A., Mojsilović, S., Ilić, V.,& Bugarski, D.. (2013). Interleukin-17 modulates myoblast cell migration by inhibiting urokinase type plasminogen activator expression through p38 mitogen-activated protein kinase. in International Journal of Biochemistry & Cell Biology Pergamon-Elsevier Science Ltd, Oxford., 45(2), 464-475. https://doi.org/10.1016/j.biocel.2012.11.010
Krstić J, Santibanez JF, Krstić A, Mojsilović S, Ilić V, Bugarski D. Interleukin-17 modulates myoblast cell migration by inhibiting urokinase type plasminogen activator expression through p38 mitogen-activated protein kinase. in International Journal of Biochemistry & Cell Biology. 2013;45(2):464-475. doi:10.1016/j.biocel.2012.11.010 .
Krstić, Jelena, Santibanez, Juan F., Krstić, Aleksandra, Mojsilović, Slavko, Ilić, Vesna, Bugarski, Diana, "Interleukin-17 modulates myoblast cell migration by inhibiting urokinase type plasminogen activator expression through p38 mitogen-activated protein kinase" in International Journal of Biochemistry & Cell Biology, 45, no. 2 (2013):464-475, https://doi.org/10.1016/j.biocel.2012.11.010 . .