Selected Publication:
SHR
Neuro
Cancer
Cardio
Lipid
Metab
Microb
Kocić, J; Santibañez, 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.
Int J Biochem Cell Biol. 2013; 45(2): 464-475.
Doi: 10.1016/j.biocel.2012.11.010
Web of Science
PubMed
FullText
FullText_MUG
- Leading authors Med Uni Graz
-
Krstic Jelena
- Altmetrics:
- Dimensions Citations:
- Plum Analytics:
- Scite (citation analytics):
- 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.
Copyright © 2012 Elsevier Ltd. All rights reserved.
- Find related publications in this database (using NLM MeSH Indexing)
-
Actin Cytoskeleton - metabolism
-
Animals -
-
Cell Differentiation -
-
Cell Line -
-
Cell Movement -
-
Cell Proliferation -
-
Down-Regulation -
-
Enzyme Activation -
-
Extracellular Signal-Regulated MAP Kinases - metabolism
-
Imidazoles - pharmacology
-
Interleukin-17 - physiology
-
MAP Kinase Signaling System -
-
Mice -
-
Myoblasts - physiology
-
Pyridines - pharmacology
-
Transcriptional Activation -
-
Urokinase-Type Plasminogen Activator - genetics
-
Urokinase-Type Plasminogen Activator - metabolism
-
p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors
-
p38 Mitogen-Activated Protein Kinases - metabolism
- Find related publications in this database (Keywords)
-
Myoblast
-
IL-17
-
p38
-
uPA
-
Migration
-
Differentiation