Apelin stimulates proliferation and suppresses apoptosis of mouse osteoblastic cell line MCM-E1 via JNK and PI3-K/Akt signaling pathways

作者：Tang, Si-Yuan; Xie, Hui; Yuan, Ling-Qing; Luo, Xiang-Hang; Huang, Jiao; Cui, Rong-Rong; Zhou, Hou-De; Wu, Xian-Ping; Liao, Er-Yuan^*

来源：Peptides, 2007, 28(3): 708-718.

DOI：10.1016/j.peptides.2006.10.005

• apelin
• osteoblast
• proliferation
• apoptosis

The aim of this study was to investigate the effects of apelin on proliferation and apoptosis of mouse osteoblastic MC3T3-E1 cells. APJ was expressed in MC3T3-E1 cells. Apelin did not affect Runx2 expression, alkaline phosphatase (ALP) activity, osteocalcin and type I collagen secretion, suggesting that it has no effect on osteoblastic differentiation of MC3T3-E1 cells. However, apelin stimulated MC3T3-E1 cell proliferation and inhibited cell apoptosis induced by serum deprivation. Our study also shows that apelin decreased cytochrome c release and caspase-3, capase-8 and caspase-9 activation in serum-deprived MC3T3-E1 cells. Apelin activated c-jun N-terminal kinase (JNK) and Akt (phosphatidylinositol 3-kinase downstream effector), and the JNK inhibitor SP600125, the phosphatidylinositol 3-kinase (PI3-K) inhibitor LY294002 or the Akt inhibitor 1L-6-hydroxymethyl-chiro-inositol 2-(R)-2-O-methyl-3-O-octadecylcarbonate (HIMO) inhibited its effects on proliferation and serum deprivation-induced apoptosis. Furthermore, apelin protected against apoptosis induced by the glucocorticoid dexamethasone or TNF-alpha. Apelin stimulates proliferation and suppresses serum deprivation-induced apoptosis of MC3T3-E1 cells and these actions are mediated via JNK and PI3-K/Akt signaling pathways.

• 出版日期2007-3
• 单位中南大学