表皮生长因子受体在凝血酶调节血管平滑肌细胞增殖中的作用

K. Smiljanic, I. Resanović, K. Savić, A. Jovanović, S. Zafirovic, M. Obradović, E. Isenovic
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引用次数: 0

摘要

动脉粥样硬化、高血压和再狭窄等血管疾病发生的共同因素是血管壁内(内膜)层血管平滑肌细胞(VSMC)的过度积累和增殖。凝血酶在动脉粥样硬化病变中介导血管通透性和收缩、VSMC的迁移和增殖,吸引单核细胞和多种促炎标志物,是动脉粥样硬化迷宫中的关键角色。凝血酶可以直接作为丝氨酸蛋白酶和/或通过激活其G蛋白偶联受体(GPCR)发挥作用。研究表明,凝血酶可介导VSMC增殖过程中表皮生长因子受体(EGFR)的反活化。EGFR的反式活化过程通过凝血酶蛋白酶活化受体(PAR)的活化,包括基质金属蛋白酶裂解膜配体前体如表皮生长因子样生长因子结合肝素(HB-EGF)与EGFR结合并激活其,通过丝裂原活化蛋白激酶(MAPK)的下游信号通路导致VSMC增殖。本文综述了近年来有关EGFR激活介导凝血酶在VSMC中增殖作用的最新文献资料,并对凝血酶刺激EGFR反激活在VSMC增殖机制中的三重级联概念进行了认识。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Role of the epidermal growth factor receptor in thrombin regulated vascular smooth muscle cells proliferation
The common factor in the development of vascular diseases, such as atherosclerosis, hypertension and restenosis, is excessive accumulation and proliferation of vascular smooth muscle cells (VSMC) within inner (intima) layer of vessel wall. Thrombin, a key player in athero-coagulation maze, mediates the regulation of vascular permeability and contraction, migration and proliferation of VSMC, attracting monocytes and a variety of proinflammatory markers in atherosclerotic lesions. Thrombin exerts its effects either directly as serine proteinases and/or via activation of its G proteins coupled receptors (GPCR). It has been shown that thrombin mediates transactivation of epidermal growth factor receptor (EGFR) within the process of VSMC proliferation. EGFR transactivation process through the activation of thrombin protease activated receptor (PAR), includes a matrix metalloproteinase cleavage of membrane ligands precursors such as epidermal growth factor like growth factor that binds heparin (HB-EGF) that binds to the EGFR and activates it, leading to VSMC proliferation via downstream signaling pathways of mitogen activated protein kinase (MAPK). This review article presents review of the new literature data concerning: the role of EGFR activation in mediating the proliferative effect of thrombin in VSMC and understanding of the concept of the triple cascade of EGFR transactivation stimulated by thrombin in the mechanism of VSMC proliferation.
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