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色氨酸蛋白在人血管内皮细胞中形成储存式阳离子通道。

Trp proteins form store-operated cation channels in human vascular endothelial cells.

作者信息

Groschner K, Hingel S, Lintschinger B, Balzer M, Romanin C, Zhu X, Schreibmayer W

机构信息

Institut für Pharmakologie und Toxikologie, Karl-Franzens-Universität Graz, Austria.

出版信息

FEBS Lett. 1998 Oct 16;437(1-2):101-6. doi: 10.1016/s0014-5793(98)01212-5.

DOI:10.1016/s0014-5793(98)01212-5
PMID:9804180
Abstract

Members of the Trp protein family have been suggested as the structural basis of store-operated cation conductances. With this study, we provide evidence for the expression of three isoforms of Trp (hTrp1, 3 and 4) in human umbilical vein endothelial cells (HUVEC). The role of Trp proteins in store regulation of endothelial membrane conductances was tested by expression of an N-terminal fragment of hTrp3 (N-TRP) which exerts a dominant negative effect on Trp channel function presumably due to suppression of channel assembly. Depletion of intracellular Ca2+ stores with IP3 (100 microM) or thapsigargin (100 nM) induced a substantial cation conductance in sham-transfected HUVEC as well as in HUVEC transfected with hTrp3. In contrast, HUVEC transfected with N-TRP failed to exhibit store-operated currents. Our results suggest the involvement of Trp related proteins in the store-operated cation conductance of human vascular endothelial cells.

摘要

已有人提出,瞬时受体电位(Trp)蛋白家族成员是储存调控性阳离子电导的结构基础。在本研究中,我们提供了人脐静脉内皮细胞(HUVEC)中三种Trp亚型(hTrp1、3和4)表达的证据。通过表达hTrp3的N端片段(N-TRP)来测试Trp蛋白在内皮细胞膜电导储存调控中的作用,该片段可能由于抑制通道组装而对Trp通道功能产生显性负效应。用肌醇三磷酸(IP3,100微摩尔)或毒胡萝卜素(100纳摩尔)耗尽细胞内Ca2+储存,可在假转染的HUVEC以及转染hTrp3的HUVEC中诱导出大量阳离子电导。相比之下,转染N-TRP的HUVEC未能表现出储存调控性电流。我们的结果表明,Trp相关蛋白参与了人血管内皮细胞的储存调控性阳离子电导。

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