Vibration loading promotes osteogenic differentiation of bone marrow-derived mesenchymal stem cells via p38 MAPK signaling pathway

被引:29
作者
Lu, Yuezhi [1 ,2 ]
Zhao, Qian [1 ,2 ]
Liu, Yang [1 ]
Zhang, Ling [1 ,2 ]
Li, Danxue [1 ,2 ]
Zhu, Zhuoli [2 ]
Gan, Xueqi [1 ,2 ]
Yu, Haiyang [1 ,2 ]
机构
[1] Sichuan Univ, West China Sch Stomatol, State Key Lab Oral Dis, Chengdu, Sichuan, Peoples R China
[2] Sichuan Univ, West China Sch Stomatol, Dept Prosthodont, Chengdu, Sichuan, Peoples R China
基金
中国国家自然科学基金;
关键词
Low magnitude high frequency vibration; Osteogenic differentiation; Proliferation; Bone marrow-derived mesenchymal stem cells; p38; MAPK; WHOLE-BODY VIBRATION; HIGH-FREQUENCY; STROMAL CELLS; LOW-MAGNITUDE; SHEAR-STRESS; PROLIFERATION; MAINTENANCE; WOMEN;
D O I
10.1016/j.jbiomech.2018.01.039
中图分类号
Q6 [生物物理学];
学科分类号
071011 ;
摘要
Low magnitude high frequency vibration (LMHFV) exhibits effectively anabolic effects on the bone tissue, and can promote osteogenic differentiation of mesenchymal stem cells (MSCs) in vitro. The role of p38 MAPK signaling in LMHFV-induced osteogenesis remains unclear. In this current study, LMHFV loading was applied to BMSCs in vitro, and cell proliferation, alkaline phosphatase (ALP), matrix mineralization, as well as osteogenic genes expression were assayed. The mechanism of mechanical signal transduction was analysed using PCR array, qRT-PCR and Western blot. LMHFV increased cell proliferation in the growth medium, while inhibited proliferation in the osteogenic medium. ALP activity, matrix mineralization and osteogenic genes expression of Runx2, Col-I, ALP, OPN and OC were increased by LMHFV. p38 and MKK6 genes expression, and p38 phosphorylation were promoted in LMHFV-induced osteogenesis. Inhibition of p38 MAPK with SB203580 and targeted p38 siRNA blunted the increased ALP activity and osteogenic genes expression by LMHFV. These findings suggest that LMHFV promotes osteogenic differentiation of BMSCs, and p38 MAPK signaling shows an important function in LMHFV-induced osteogenesis. (C) 2018 Elsevier Ltd. All rights reserved.
引用
收藏
页码:67 / 75
页数:9
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