Follistatin could promote the proliferation of duck primary myoblasts by activating PI3K/Akt/mTOR signalling.

Xinxin Li,Fang Ding,Hehe Liu,Jiwen Wang,Lingli Sun,Wenqiang Sun,Chunchun Han,Haohan Wang

doi:10.1042/bsr20140085

Xinxin Li, Fang Ding + Show 6 more

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https://doi.org/10.1042/bsr20140085

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Journal: Bioscience reports	Publication Date: Oct 1, 2014
Citations: 16	License type: CC BY 3.0

Affiliation: Sichuan Agricultural University

Abstract

FST (follistatin) is essential for skeletal muscle development, but the intracellular signalling networks that regulate FST-induced effects are not well defined. We sought to investigate whether FST promotes the proliferation of myoblasts through the PI3K (phosphoinositide 3-kinase)/Akt (protein kinase B)/mTOR (mammalian target of rapamycin) signalling. In the present study, we transfected the pEGFP-duFST plasmid and added PI3K and mTOR inhibitors to the medium of duck primary myoblasts. Then, we analysed the cellular phenotypic changes that occurred and analysed 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 S6K (S6 kinase) and the protein expression of phospho-Akt (Thr308), mTOR, phospho-mTOR (serine 2448), phospho-S6K (Ser417), inhibited the mRNA expression of FoxO1, MuRF1 (muscle RING finger-1) 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 signalling. In light of the present results, we hypothesize that duck FST could promote myoblast proliferation, which is dependent on PI3K/Akt/mTOR signalling.

Highlights

FST, a single-chain monomeric glycoprotein, plays an important function in embryogenesis, muscle development and adult life [1,2]
We used a duck model to investigate the functions of FST in birds, and our results were consistent with the previous research in mammals, demonstrating a similar role of FST in regulating myoblast proliferation (Figure 1)
FST is an important extracellular protein, and it has been shown to regulate the expression of protein kinase B (Akt)/mammalian target of rapamycin (mTOR) signalling through insulin-like growth factor (IGF)-1R, which resulted in phenotypic changes in skeletal muscle [6,27]

Summary

Introduction

FST (follistatin), a single-chain monomeric glycoprotein, plays an important function in embryogenesis, muscle development and adult life [1,2]. It was shown that FST is important in promoting myoblast proliferation and differentiation in vitro studies [5]. Some scholars have shown that FST could promote skeletal muscle hypertrophy in mice by activating IGF-1R (type 1 insulin-like growth factor receptor)/Akt (protein kinase B) signalling and inhibiting MSTN (myostatin) signalling [6,7]. In birds, the information about FST in muscle development has not been well studied. Previous studies in our laboratory showed that recombinant duck FST protein could promote muscle hypertrophy in the post-hatching duck by inducing satellite cell proliferation [8]. The regulatory mechanism of FST in the skeletal muscle development of birds remains an open question

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