MiR‐222‐3p suppresses C2C12 myoblast proliferation and differentiation via the inhibition of IRS‐1/PI3K/Akt pathway

Abstract

Numerous studies have revealed the profound impact of microRNAs on regulating skeletal muscle development and regeneration. However, the biological function and regulation mechanism of miR‐222‐3p in skeletal muscle remains largely unknown. In this study, miR‐222‐3p was found to be abundantly expressed in the impaired skeletal muscles, indicating that it might have function in the development and regeneration process of the skeletal muscle. MiR‐222‐3p overexpression impeded C2C12 myoblast proliferation and myogenic differentiation, whereas inhibition of miR‐222‐3p got the opposite results. The dual‐luciferase reporter assay showed that insulin receptor substrate‐1 (IRS‐1) was the target gene of miR‐222‐3p. We next found that knockdown of IRS‐1 could obviously suppress C2C12 myoblast proliferation and differentiation. Additionally, miR‐222‐3p‐induced repression of myoblast proliferation and differentiation was verified to be associated with a decrease in phosphoinositide 3‐kinase (PI3K)‐Akt signaling. Overall, we demonstrated that miR‐222‐3p inhibited C2C12 cells myogenesis via IRS‐1/PI3K/Akt pathway. Therefore, miR‐222‐3p may be used as a therapeutic target for alleviating muscle loss caused by inherited and nonhereditary diseases.

Transcriptome Analysis of miRNA and mRNA in Porcine Skeletal Muscle following Glaesserella parasuis Challenge

“…miRNAs are small non-coding RNAs that act as inhibitors of gene expression and play important roles in skeletal muscle development. Several miRNAs, including muscle-specific miRNAs such as those of the miR-1/miR-206 and miR-133a/miR-133b families [ 15 , 16 , 17 , 18 ], as well as miRNAs including miR-17 [ 19 ], miR-22 [ 20 ], miR-29 [ 21 ], miR-136 [ 20 ], miR-186 [ 22 ], miR-204 [ 23 ], and miR-222 [ 24 ], have been implicated in skeletal muscle development through their regulation of target genes. Muscle atrophy occurs when the rate of protein degradation exceeds protein synthesis, often induced by factors such as starvation and disease conditions.…”

Role of TRPC6 in apoptosis of skeletal muscle ischemia/reperfusion injury

“…Additionally, they found that and Ca 2+ can in uenceaffect the phosphatidylinositol 3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/Akt/mTOR) pathway to alleviate pulmonary hypertension. TheMeanwhile, PI3K/Akt/mTOR signalling pathway is an important cellular transduction pathway in cells, thatwhich can promotes cell proliferation and differentiation, therebyus regulating cell growtWTh [20][21][22]. ThereforeBased on the above, wethis study aimed to establish and verify the effect of IRI on the expression of the PI3K/Akt/mTOR signalling pathway and apoptosis of skeletal muscle cells in the absence of the TRPC6 pathway in skeletal muscle.…”