CTRP3/cartducin promotes proliferation and migration of endothelial cells
CTRP3/cartducin promotes proliferation and migration of endothelial cells
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DOI：
10.1007/s11010-007-9506-6
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发表时间：
2007-10-01
影响因子：
4.3
通讯作者：
Maeda, Takashi
中科院分区：
文献类型：
--
作者：
Akiyama, Hironori;Furukawa, Souhei;Maeda, Takashi
CTRP 3/cartducin是一种新的分泌蛋白，属于C1 q和肿瘤坏死因子相关蛋白（CTRP）超家族成员。CTRP 3/cartducin基因在球囊损伤大鼠颈动脉组织中瞬时上调在这项研究中，我们报告了CTRP 3/cartducin作为血管生成过程调节剂的新功能。CTRP 3/cartducin以剂量依赖性方式促进小鼠内皮MSS 31细胞的增殖和迁移。此外，通过CTRP 3/cartducin刺激MSS 31导致细胞外信号调节激酶1/2（ERK 1/2）和p38丝裂原活化蛋白激酶（MAPK）的活化。MAPK/ERK激酶1/2（MEK 1/2）抑制剂U 0126和p38 MAPK抑制剂SB 203580可阻断CTRP 3/cartducin诱导的细胞增殖，U 0126可阻断细胞迁移，但SB 203580不能。总之，这些结果表明，CTRP 3/cartducin可能作为一种新的血管生成因子参与血管成形术后新生内膜的形成。
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.