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SHR Neuro Cancer Cardio Lipid Metab Microb

Obradović, H; Krstić, J; Kukolj, T; Trivanović, D; Đorđević, IO; Mojsilović, S; Jauković, A; Jovčić, G; Bugarski, D; Santibañez, JF.
Doxycycline Inhibits IL-17-Stimulated MMP-9 Expression by Downregulating ERK1/2 Activation: Implications in Myogenic Differentiation.
Mediators Inflamm. 2016; 2016(1): 2939658-2939658. Doi: 10.1155/2016/2939658 [OPEN ACCESS]
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Co-authors Med Uni Graz
Krstic Jelena
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Abstract:
Interleukin 17 (IL-17) is a cytokine with pleiotropic effects associated with several inflammatory diseases. Although elevated levels of IL-17 have been described in inflammatory myopathies, its role in muscle remodeling and regeneration is still unknown. Excessive extracellular matrix degradation in skeletal muscle is an important pathological consequence of many diseases involving muscle wasting. In this study, the role of IL-17 on the expression of matrix metalloproteinase- (MMP-) 9 in myoblast cells was investigated. The expression of MMP-9 after IL-17 treatment was analyzed in mouse myoblasts C2C12 cell line. The increase in MMP-9 production by IL-17 was concomitant with its capacity to inhibit myogenic differentiation of C2C12 cells. Doxycycline (Doxy) treatment protected the myogenic capacity of myoblasts from IL-17 inhibition and, moreover, increased myotubes hypertrophy. Doxy blocked the capacity of IL-17 to stimulate MMP-9 production by regulating IL-17-induced ERK1/2 MAPK activation. Our results imply that MMP-9 mediates IL-17's capacity to inhibit myoblast differentiation during inflammatory diseases and indicate that Doxy can modulate myoblast response to inflammatory induction by IL-17.
Find related publications in this database (using NLM MeSH Indexing)
Animals -
Cell Differentiation -
Cell Line -
Doxycycline - chemistry
Gene Expression Regulation -
Inflammation -
Interleukin-17 - metabolism
MAP Kinase Signaling System -
Matrix Metalloproteinase 9 - metabolism
Mice -
Muscle Development -
Muscle, Skeletal - metabolism
Myoblasts - cytology
Myoblasts - metabolism
Recombinant Proteins - metabolism

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