CTRP3/cartducin promotes proliferation and migration of endothelial cells

被引：69
|
作者：
Akiyama, Hironori
Furukawa, Souhei
Wakisaka, Satoshi
Maeda, Takashi
机构：
[1] Osaka Univ, Grad Sch Dent, Dept Anat & Cell Biol, Suita, Osaka 5650871, Japan
[2] Osaka Univ, Grad Sch Dent, Dept Radiol, Suita, Osaka 5650871, Japan
来源：
MOLECULAR AND CELLULAR BIOCHEMISTRY | 2007年 / 304卷 / 1-2期
关键词：
CTRP3; cartducin; endothelial cells; proliferation; migration; MAPK;
D O I：
10.1007/s11010-007-9506-6
中图分类号：
Q2 [细胞生物学];
学科分类号：
071009 ; 090102 ;
摘要：
CTRP3/cartducin, a novel secretory protein, is a member of the C1q and tumor necrosis factor (TNF)-related protein (CTRP) superfamily. CTRP3/cartducin gene is transiently up-regulated in a balloon-injured rat carotid artery tissue. In this study, we report a new function of CTRP3/cartducin as a regulator of angiogenic processes. CTRP3/cartducin promoted proliferation and migration of mouse endothelial MSS31 cells in a dose-dependent manner. Further, stimulation of MSS31 by CTRP3/cartducin led to activation of extracellular signal-regulated kinase 1/2 (ERK1/2) and p38 mitogen-activated protein kinase (MAPK). MAPK/ERK kinase 1/2 (MEK1/2) inhibitor, U0126, and p38 MAPK inhibitor, SB203580, blocked the CTRP3/cartducin-induced cell proliferation, and migration was blocked by U0126, but not the SB203580. Taken together, these results suggest that CTRP3/cartducin may be involved as a novel angiogenic factor in the formation of neointima following angioplasty.
引用
收藏
页码：243 / 248
页数：6
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