期刊
CYTOKINE
卷 60, 期 3, 页码 646-652出版社
ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.cyto.2012.07.033
关键词
Chemerin; C2C12 cells; ERK1/2; mTOR
资金
- NSFC [31001015]
- National Basic Research Program of China [2012CB124704]
- State Key Laboratory of Animal Nutrition [2004DA125184 F1113]
- Chinese Academy of Sciences and Knowledge Innovation Project [KZCX2-EW-412]
- Project of Institute of Subtropical Agriculture, Chinese Academy of Sciences [ISACX-LYQY-QN-1104]
Obesity in human is an alarming major public health crisis worldwide and insulin resistance is a hallmark of it. The negative cross-talk between skeletal muscle and adipose tissue through adipokines is now accepted as one of the leading cause of insulin resistance. Chemerin is a novel adipokine previously reported to induce insulin resistance in primary human skeletal muscle cells. To investigate the role of chemerin in myogenesis, C2C12 cells were used and treated with chemerin in proliferation and differentiation stages. Our results showed that chemerin promoted proliferation and suppressed differentiation of C2C12 cells through extracellular-signal regulated kinase-1/2 (ERK1/2) and mammalian target of rapamycin (mTOR) signaling pathways, and these two pathways were interacted with each other in C2C12 cells treated with chemerin. It is concluded from this in vitro study that chemerin which expression is increased during myoblast differentiation appears to be able, likely in an autocrine/paracrine manner, to increase myoblast proliferation and decrease myoblast differentiation. (c) 2012 Elsevier Ltd. All rights reserved.
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