Inhibition of adipogenic differentiation by myostatin is alleviated by arginine supplementation in porcine-muscle-derived mesenchymal stem cells
Inhibition of adipogenic differentiation by myostatin is alleviated by arginine supplementation in porcine-muscle-derived mesenchymal stem cells
复制标题
在猪肌肉来源的间充质干细胞中补充精氨酸可减轻肌肉生长抑制素对脂肪形成分化的抑制
DOI:
10.1007/s11427-011-4227-1
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发表时间:
2011-10-01
影响因子:
9.1
通讯作者:
Chen DaiWen
中科院分区:
文献类型:
--
作者:
Lei HuLong;Yu Bing;Chen DaiWen
Porcine mesenchymal stem cells in postnatal muscle have been demonstrated to differentiate into adipocytes. This increases adipocyte number and lipid accumulation, and is thought to be the origin of intramuscular fat. In this study, the effects of myostatin and arginine on adipogenic differentiation in mesenchymal stem cells derived from porcine muscle (pMDSCs) were investigatedin vitro. Intracellular triglyceride levels were reduced by exogenous myostatin and increased by arginine supplementation or myostatin antibody (P<0.01). The inhibition of lipid accumulation by myostatin in pMDSCs was alleviated by arginine supplementation (P<0.01). Expression patterns of adipogenic transcription factors showed that exogenous myostatin suppressedPPARγ2andaP2expression (P<0.01), while supplemental arginine or myostatin antibody promotedADD1expression (P<0.01). Furthermore, compared with the addition of either myostatin protein or antibody alone,ADD1andPPARδexpression were promoted by the combination of arginine and myostatin (P<0.01), and arginine combined with myostatin antibody promoted the expression ofADD1, PPARδ, C/EBPα, PPARγ2andLPLin pMDSCs (P<0.05). These results suggest that myostatin inhibits adipogenesis in pMDSCs, and that this can be alleviated by arginine supplementation, at least in part, through promotingADD1andPPARδexpression.