MiR-147 inhibits cyclic mechanical stretch-induced apoptosis in L6 myoblasts via ameliorating endoplasmic reticulum stress by targeting BRMS1.

Abstract

Functional orthopedic treatment is effective for the correction of malformation. Studies demonstrated myoblasts undergo proliferation and apoptosis on certain stretch conditions. MicroRNAs (miRNAs) function in RNA silencing and post-transcriptional regulation of gene expression, and participate in various biological processes, including proliferation and apoptosis. One hypothesis suggested that miRNA was involved into the procedure via suppressing its target genes then triggered endoplasmic reticulum stress-induced apoptosis. Therefore, miRNAs play important roles in the regulation of the proliferation and apoptosis of myoblasts. In our study, the miR-147 has been explored. A cyclic mechanical stretch model was established to observe the features of rat L6 myoblasts. The detection of mRNA and protein levels was performed by qRT-PCR and western blot. L6 cell proliferation/apoptosis was checked by CCK-8 assay, DNA fragmentation assay, and caspase-3 activity assay. MiRNA transfections were performed as per the manufacturer's suggestions: (1) cyclic mechanical stretch induced apoptosis of L6 myoblasts and inhibition of miR-147; (2) miR-147 attenuated cyclic mechanical stretch-induced apoptosis of L6 myoblasts; (3) miR-147 attenuated cyclic mechanical stretch-induced L6 myoblast endoplasmic reticulum stress; (4) BRMS1 was a direct target of miR-147 in L6 myoblasts; (5) miR-147/BRMS1 axis participated in the regulation of cyclic mechanical stress on L6 myoblasts. MiR-147 attenuates endoplasmic reticulum stress by targeting BRMS1 to inhibit cyclic mechanical stretch-induced apoptosis of L6 myoblasts.