H(2)O(2)激活的TRPM2钙通道在氧化剂诱导的内皮损伤中的作用
Role of H(2)O(2)-activated TRPM2 calcium channel in oxidant-induced endothelial injury.
作者信息
Hecquet Claudie M, Malik Asrar B
机构信息
Department of Pharmacology, University of Illinois at Chicago, Chicago, Illinois, USA.
出版信息
Thromb Haemost. 2009 Apr;101(4):619-25.
Abstract
The transient receptor potential (melastatin) 2 (TRPM2), is an oxidant-activated non-selective cation channel that is widely expressed in mammalian tissues including the vascular endothelium. Oxidative stress, through the generation of oxygen metabolites including H(2)O(2), stimulates intracellular ADP-ribose formation which, in turn, opens TRPM2 channels. These channels act as an endogenous redox sensor for mediating oxidative stress/ROS-induced Ca(2+) entry and the subsequent specific Ca(2+)-dependent cellular reactions such as endothelial hyperpermeability and apoptosis. This review summarizes recent findings on the mechanism by which oxidants induce TRPM2 activation, the role of these channels in the signalling vascular endothelial dysfunctions, and the modulation of oxidant-induced TRPM2 activation by PKCalpha and phospho-tyrosine phosphates L1.
摘要
瞬时受体电位（褪黑素）2（TRPM2）是一种氧化剂激活的非选择性阳离子通道，广泛表达于包括血管内皮在内的哺乳动物组织中。氧化应激通过产生包括H(2)O(2)在内的氧代谢产物，刺激细胞内ADP-核糖的形成，进而打开TRPM2通道。这些通道作为内源性氧化还原传感器，介导氧化应激/活性氧诱导的Ca(2+)内流以及随后特定的Ca(2+)依赖性细胞反应，如内皮细胞高通透性和凋亡。本综述总结了关于氧化剂诱导TRPM2激活的机制、这些通道在血管内皮功能障碍信号传导中的作用以及蛋白激酶Cα和磷酸酪氨酸磷酸酶L1对氧化剂诱导的TRPM2激活的调节的最新研究发现。
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