Chemerin regulates proliferation and differentiation of myoblast cells via ERK1/2 and mTOR signaling pathways

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.

► Differentiation markedly induced chemerin mRNA in C2C12 cells. ► Chemerin promoted C2C12 cells proliferation through ERK1/2. ► Chemerin inhibited C2C12 cells differentiation through ERK1/2. ► mTOR involved in regulating proliferation and differentiation of C2C12 cells by chemerin. ► ERK1/2 and mTOR interacted with each other in C2C12 cells.