Biomechanical Stretch Induces Inflammation, Proliferation, and Migration by Activating NFAT5 in Arterial Smooth Muscle Cells

被引:22
作者
Cao, Wei [1 ,2 ]
Zhang, Donghui [1 ,2 ]
Li, Qiannan [3 ]
Liu, Yue [4 ]
Jing, Shenhong [1 ,2 ]
Cui, Jinjin [1 ,2 ]
Xu, Wei [1 ,2 ]
Li, Shufeng [1 ,2 ]
Liu, Jingjin [1 ,2 ]
Yu, Bo [1 ,2 ]
机构
[1] Harbin Med Univ, Dept Cardiol, Affiliated Hosp 2, Harbin 150086, Heilongjiang, Peoples R China
[2] Chinese Minist Educ, Key Lab Myocardial Ischemia, Harbin 150081, Heilongjiang, Peoples R China
[3] Harbin Med Univ, Dept Geriatr, Affiliated Hosp 2, Harbin 150081, Heilongjiang, Peoples R China
[4] Harbin Med Univ, Affiliated Hosp 1, Dept Cardiol, Harbin 150001, Heilongjiang, Peoples R China
基金
中国国家自然科学基金;
关键词
inflammation; proliferation; migration; NFAT5; arterial smooth muscle cells; GENE-EXPRESSION; HYPERTENSION; MYOCARDIN; NFAT5/TONEBP; DIFFERENTIATION; HYPERPLASIA; MECHANISM; RAT;
D O I
10.1007/s10753-017-0653-y
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
The increasing wall stress as is elicited by arterial hypertension promotes their reorganization in the vessel wall which may lead to arterial stiffening and contractile dysfunction. The nuclear factor of activated T cells 5 (NFAT5) pathway plays a role in regulating growth and differentiation in various cell types. We investigated whether the NFAT5 pathway was involved in the regulation of biomechanical stretch-induced human arterial smooth muscle cell (HUASMC) proliferation, inflammation, and migration. Herein, we showed that stretch promoted the expression of NFAT5 in human arterial smooth muscle cells and regulated through activation of c-Jun N-terminal kinase under these conditions. This may contribute to an improved activity of HUASMCs and thus promote reorganization in vascular remodeling processes such as hypertension-induced arterial stiffening and contractile dysfunction.
引用
收藏
页码:2129 / 2136
页数:8
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