Fp329urotensin Ii Induces Mice Skeletal Autophagy Via Enhancing Skeletal Muscle Cell Autophagy and Affecting Irisin Precusor(fndc5) Expression
Year: 2018
Type: conference-abstract
Abstract: INTRODUCTION AND AIMS: Plasma urotensin II(UII) and tissue urotensin II expression were higher in chronic renal failure. We hypothesized that UII may induce skeletal muscle atrophy by inhibiting the irisin precusor FNDC5 expression or enhancing skeletal autophagy via many mechanisms. METHODS: Mouse skeletal muscle cells (C2C12) were differentiate by 2% horse serum ,and were exposed to different concentrations UII (10-5M-10-7M) for 6-12h, then expressions of LC3II and p62,irisin prescusor (FNDC5) were detected by western blot. Moreover,expressions of UII, FNDC5, LC3II, p62 in skeletal muscle tissues for three animal model (the sham operation mice as normal control group, wild type C57Bl/6 mice with 5/6 nephrectomy as wild type chronic renal failure group (WTCRF),UII receptor gene knock out combined with 5/6 nephrectomy(UTKOCRF))were performed via immunohistochemical staining and western blot. RESULTS: UII directly induced mouse skeletal muscle cells autophagy without dose-dependent and time-depedent, and the optimal action was UII with 10-7M, but UII did not down-regulate the expression of FNDC5 at the same time. WTCRF mice had lower both limb weight compared with normal control, while UII receptor gene knock mice had higher both limb weight;moreover, the upregulation of skeletal muscle tisse autophagy markers were inhibited, and the decreased expression FNDC5 in WTCRF were reversed. CONCLUSIONS: UII could induce skeletal muscle atrophy via directly enhacing skeletal mucle cell autophagy by vitro and vivo study, although we cannot verify UII inhibit irisin precursor (FNDC5) in vitro C2C12 cells, but in vivo animal study, we demonstrated that interfering UII action (UII receptor gene knock out) can upregulate irisin precusor FNDC5 expression.
Authors: Ya Jing Pan, Si-Ruo Guo, Meng-Ze Zhang, Lin-Hui He, Ai-Hua Zhang
Institutions: Peking University, Peking University Third Hospital
Language: English
Subfield: Molecular Biology
Domain: Life Sciences
Open Access status: bronze
OpenAlex ID: W2804125089