17β-estradiol represses myogenic differentiation by increasing ubiquitin-specific peptidase 19 through estrogen receptor α.

ABSTRACT: Skeletal muscles express estrogen receptor (ER) α and ERβ. However, the roles of estrogens acting through the ERs in skeletal muscles remain unclear. The effects of 17β-estradiol (E2) on myogenesis were studied in C2C12 myoblasts. E2 and an ERα-selective agonist propylpyrazole-triol depressed myosin heavy chain (MHC), tropomyosin, and myogenin levels and repressed the fusion of myoblasts into myotubes. ER antagonist ICI 182,780 cancelled E2-repressed myogenesis. E2 induced ubiquitin-specific peptidase 19 (USP19) expression during myogenesis. E2 replacement increased USP19 expression in the gastrocnemius and soleus muscles of ovariectomized mice. Knockdown of USP19 inhibited E2-repressed myogenesis. Mutant forms of USP19 lacking deubiquitinating activity increased MHC and tropomyosin levels

SUBMITTER: Ogawa M 

PROVIDER: S-EPMC3308857 | biostudies-literature | 2011 Dec

REPOSITORIES: biostudies-literature