Concomitant activation of the PI3K/Akt and ERK1/2 signalling is involved in cyclic compressive force‐induced IL‐6 secretion in MLO‐Y4 cells. (10th January 2014)

• Record Type: Journal Article
• Authors: Yin, Jian; Hao, Zhichao; Ma, Yuanyuan; Liao, Shuang; Li, Xianxian; Fu, Jing; Wu, Yeke; Shen, Jiefei; Zhang, Ping; Li, Xiaoyu; Wang, Hang
• Is Part Of: Cell biology international. Volume 38:Number 5(2014)
• Page Start: 591
• Page End: 598
• Publication Date: 2014-01-10
• Subjects: Cytology -- Periodicals; Cells -- Periodicals; 571.605
• DOI: 10.1002/cbin.10235
• Languages: English
• ISSNs: 1065-6995

Abstract

<abstract abstract-type="main" xml:lang="en"> <title>Abstract</title> <sec id="cbin10235-sec-0001" sec-type="section"> <p>IL‐6 has a dual role in bone remodelling. The ERK1/2 pathway partially upregulated IL‐6 secretion in osteocyte‐like MLO‐Y4 cells exposed to CCF. We have now investigated the possible role of phosphatidylinositol 3‐kinase (PI3K)/Akt signalling pathway in the CCF‐induced IL‐6 expression. MLO‐Y4 cells were treated with CCF 2, 000 µstrain, 2 Hz, or 10, 30 min, 1, 3 and 6 h. IL‐6 expression, Akt and ERK1/2 and PI3K/Akt phosphorylation were determined by RT‐PCR, ELISA and Western blotting. Inhibition of PI3K/Akt with LY294002 or ERK1/2 with PD98059 significantly attenuated IL‐6 upregulation, and IL‐6 expression was abolished by inhibiting both pathways. Inhibition of one pathway downregulated the other's phosphorylation level. In conclusion, concomitant activation of PI3K/Akt and ERK1/2 pathways mediated IL‐6 expression in MLO‐Y4 cells under CCF.</p> </sec> </abstract>