期刊
JOURNAL OF CELLULAR BIOCHEMISTRY
卷 108, 期 5, 页码 1184-1191出版社
WILEY
DOI: 10.1002/jcb.22348
关键词
VASCULAR SMOOTH MUSCLE CELL; OSTEOBLASTIC DIFFERENTIATION; LANTHANUM; G PROTEIN; MAPK PATHWAYS
A major cellular event in vascular calcification is the phenotypic transformation of vascular smooth muscle cells (VSMCs) into osteoblast-like cells. After demonstrating that lanthanum chloride (LaCl3) suppresses hydrogen peroxide-enhanced calcification in rat calcifying vascular cells (CVCs), here we report its effect on the osteoblastic differentiation of rat VSMCs, a process leading to the formation of CVCs. Cells were isolated from aortic media of male SD rats, and passages between three and eight were cultured in Dulbeccol's Modified Eagle's Medium (DMEM) containing 10% fetal bovine serum (FBS) and 10 mM beta-glycerophosphate (beta-GP) in the presence or absence of LaCl3. Exposure of cells to LaCl3 suppressed the P-GP-induced elevations in calcium deposition, alkaline phosphatase (ALP) activity, and Cbfa1/Runx2 expression, as well as the concomitant loss of SM alpha-actin. Furthermore, LaCl3 activated the phosphorylation of extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK), and the blockage of either pathway with a specific inhibitor abolished the effects of LaCl3. In addition, pretreatment of the cells with pertussis toxin (PTx), an inhibitor of G protein-mediated signaling pathway, repealed all the changes induced by LaCl3. These findings demonstrate that LaCl3 suppresses the P-GP-induced osteoblastic differentiation and calcification in rat VSMCs, and its effect is mediated by the activation of both ERK and JNK MAPK pathways via PTx-sensitive G proteins. J. Cell. Biochem. 108: 1184-1191, 2009. (C) 2009 Wiley-Liss, Inc.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据