GSE106365
Linc-smad7 promotes myoblast differentiation and muscle regeneration via sponging miR-125b
Long noncoding RNAs (lncRNAs) are involved in the regulation of skeletal muscle development. In the present study, differentially expressed lncRNAs were identified from RNA-seq data derived from myoblasts and myotubes. We conducted studies to elucidate the function and molecular mechanism of action of Linc-smad7 during skeletal muscle development. Our findings show that Linc-smad7 is upregulated during the early phase of myoblasts differentiation. In in vitro studies, we showed that overexpression of Linc-smad7 promoted the arrest of myoblasts in G1 phase, inhibited DNA replication, and induced myoblast differentiation. Our in vivo studies suggest that Linc-smad7 stimulates skeletal muscle regeneration in cardiotoxin-induced muscle injury. Mechanistically, Linc-smad7 overexpression increased smad7 and IGF2 protein levels. On the contrary, overexpression of miR-125b reduced smad7 and IGF2 protein levels. Results of RNA immunoprecipitation analysis and biotin-labeled miR-125b capture suggest that Linc-smad7 could act as a competing endogenous RNA (ceRNA) for miRNA-125b. Taken together, our findings suggest that the novel noncoding regulator Linc-smad7 regulates skeletal muscle development. Overall design: We used RNA-seq to detect the transcriptome difference after Linc-smad7 gain of function in skeletal muscle damage. Compared to control group, existing 359 differential expressed genes, 121 genes and 238 genes were upregulated or down regulated respectively. GO analysis of genes showed that Linc-smad7 mainly participated in biological process such as skeletal muscle tissue development, skeletal muscle organ development, etc. Six skeletal muscle samples from mouse (6w) of two groups, L7 (Linc-smad7) and Control, were purchased from the Fourth Military Medical University, Xi'An, P.R. China.