CTRP3/cartducin is induced by transforming growth factor-β1 and promotes vascular smooth muscle cell proliferation
CTRP3/cartducin is induced by transforming growth factor-β1 and promotes vascular smooth muscle cell proliferation
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DOI：
10.1042/cbi20090043
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发表时间：
2010-03-01
影响因子：
3.9
通讯作者：
Wakisaka, Satoshi
中科院分区：
文献类型：
--
作者：
Maeda, Takashi;Wakisaka, Satoshi
CTRP3 (C1q和肿瘤坏死因子相关蛋白3)/cartducin是一种新型血清蛋白，是CTRP超家族的成员。尽管大鼠颈动脉球囊损伤后CTRP3/cartducin基因明显上调，但其在损伤血管动脉重塑和新生内膜形成中的生物学作用尚不清楚。我们研究了CTRP3/cartducin上调的机制以及CTRP3/cartducin对血管平滑肌细胞的体外作用。tgf - β 1（转化生长因子- β 1）可诱导培养的p53LMAC01血管平滑肌细胞中CTRP3/cartducin的表达，而bFGF（碱性成纤维细胞生长因子）或PDGF-BB（血小板衍生生长因子- bb）则不能。外源性CTRP3/cartducin通过ERK1/2（胞外信号调节激酶1/2）-和MAPK （p38丝裂原活化蛋白激酶）-信号通路以剂量依赖的方式促进p53LMAC01细胞的增殖。相比之下，CTRP3/cartducin对p53LMAC01细胞的迁移没有影响。综上所述，本研究结果表明CTRP3/导管蛋白在促进损伤后血管壁血管平滑肌细胞增殖方面具有新的生物学作用。
CTRP3 (C1q and tumour necrosis factor-related protein 3)/cartducin, a novel serum protein, is a member of the CTRP superfamily. Although the CTRP3/cartducin gene is markedly up-regulated in rat carotid arteries after balloon injury, little is known about its biological roles in arterial remodelling and neointima formation in injured blood vessels. We have investigated the mechanisms underlying CTRP3/cartducin up-regulation and the in vitro effects of CTRP3/cartducin on vascular smooth muscle cells. CTRP3/cartducin expression in cultured p53LMAC01 vascular smooth muscle cells was induced by TGF-beta 1 (transforming growth factor-beta 1), but not by bFGF (basic fibroblast growth factor) or PDGF-BB (platelet-derived growth factor-BB). Exogenous CTRP3/cartducin promoted the proliferation of p53LMAC01 cells in a dose-dependent manner via ERK1/2 (extracellular signal-regulated kinase 1/2)- and MAPK (p38 mitogen-activated protein kinase)-signalling pathways. In contrast, CTRP3/cartducin exhibited no effect on the migration of p53LMAC01 cells. Taken together, the results of the present study demonstrate a novel biological role of CTRP3/cartducin in promoting vascular smooth muscle cell proliferation in blood vessel walls after injury.