Follistatin could promote the proliferation of duck primary myoblasts by activating PI3K/Akt/mTOR signalling
| Autor: | Jiwen Wang, Fang Ding, Xinxin Li, Haohan Wang, Wenqiang Sun, Lingli Sun, Chunchun Han, Hehe Liu |
|---|---|
| Rok vydání: | 2014 |
| Předmět: |
Myoblast proliferation
Follistatin duck IGF insulin-like growth factor lcsh:Life lcsh:QR1-502 Biochemistry mTORC2 lcsh:Microbiology HRP horseradish peroxidise chemistry.chemical_compound Phosphatidylinositol 3-Kinases MTT 3-(4 5-dimethylthiazol-2-yl)-2 5-diphenyltetrazolium bromide LY294002 Cells Cultured TOR Serine-Threonine Kinases myoblasts Cell biology FST Follistatin Ducks PI3K phosphoinositide 3-kinase Myoblasts Skeletal proliferation Biophysics P70-S6 Kinase 1 mTOR mammalian target of rapamycin Biology Avian Proteins MuRF1 muscle RING finger-1 Animals MSTN myostatin Molecular Biology Protein kinase B PI3K/AKT/mTOR pathway Cell Proliferation Original Paper S6K S6 kinase RPTOR BrdU 5-bromo-2V-deoxyuridine Cell Biology Molecular biology lcsh:QH501-531 PI3K/Akt/mTOR signalling chemistry Akt protein kinase B biology.protein IGF-IR type 1 insulin-like growth factor receptor human activities Proto-Oncogene Proteins c-akt DAPI 4′ 6-diamidino-2-phenylindole |
| Zdroj: | Bioscience Reports Bioscience Reports, Vol 34, Iss 5, p e00143 (2014) |
| ISSN: | 1573-4935 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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