Different regulation role of myostatin in differentiating pig ADSCs and MSCs into adipocytes.

Bing Deng, Jianghui Wen, Yi Ding, Jian Peng, Siwen Jiang

Agricultural Ministry Key Laboratory of Swine Breeding and Genetics and Key Laboratory of Agricultural Animal Genetics, Breeding, and Reproduction of Ministry of Education, College of Animal Science and Technology, Huazhong Agricultural University, Wuhan, Hubei, China.

Cell biochemistry and function 2012 Mar

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Myostation (MSTN), which is primarily expressed in muscle, plays an important role in myogenic and adipogenic cells. However, there is little information about whether MSTN displays different roles between adipose-derived stem cells (ADSCs) and muscle satellite cells (MSCs). The two kinds of cells can both exist in the muscle and differentiate into adiposities. In this research, we isolated ADSCs and MSCs from porcine fat tissues and semitendinosus muscle, respectively, to investigate the effect of MSTN on the adipogenesis of those cells. ADSCs and MSCs were treated with recombinant human MSTN during the induction of adipogenesis or before the induction of differentiation. Then, we evaluated adipogenesis by Oil Red O staining and assessed the expression patterns of adipocyte-specific fatty acid binding protein (aP2) and peroxisome proliferator-activated receptor (PPAR) γ using real-time polymerase chain reaction methods. Our results indicated that the treatment with MSTN before or during the induction of differentiation in MSCs could both inhibit the adipogenesis. However, the treatment with MSTN only during the induction of differentiation in ADSCs could suppress the adipogenesis. Those results showed that MSTN had different roles in the adipogenesis of ADSCs and MSCs. It can shed new light on the origin of adipocyte located in muscle. Copyright © 2011 John Wiley & Sons, Ltd.

Citation

Bing Deng, Jianghui Wen, Yi Ding, Jian Peng, Siwen Jiang. Different regulation role of myostatin in differentiating pig ADSCs and MSCs into adipocytes. Cell biochemistry and function. 2012 Mar;30(2):145-50