Publication Date:
2014-09-10
Description:
Follistatin (FST) is essential for skeletal muscle development, but the intracellular signaling networks that regulate Follistatin-induced effects are not well defined. We sought to investigate whether FST promotes the proliferation of myoblasts through the phosphoinositide 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) signaling. In this study, we transfected the pEGFP-duFST plasmid and added PI3K and mTOR inhibitors to the medium of duck primary myoblasts. Then, we analyzed the cellular phenotypic changes that occurred and analyzed the expression of target genes. The results showed that FST promoted myoblast proliferation, induced the mRNA expression of PI3K, Akt, mTOR, 70-kDa ribosomal protein S6 kinase (S6K) and the protein expression of phospho-Akt (Thr308), mTOR, phospho-S6K (Ser417), inhibited the mRNA expression of FoxO1, muscle RING finger-1 (MuRF1) and the protein expression of phospho-FoxO1 (Ser256). Moreover, we found that the overexpression of FST could alleviate the inhibitory effect of myoblast proliferation caused by the addition of LY294002, a PI3K inhibitor. Additionally, the overexpression of duck FST also relieved the inhibition of myoblast proliferation caused by the addition of Rapamycin (an mTOR inhibitor) through PI3K/Akt/mTOR signaling. In light of the present results, we hypothesize that duck FST could promote myoblast proliferation, which is dependent on PI3K/Akt/mTOR signaling.
Print ISSN:
0144-8463
Electronic ISSN:
1573-4935
Topics:
Biology
,
Chemistry and Pharmacology
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