Regulation and function of TRPM7 in human endothelial cells: TRPM7 as a potential novel regulator of endothelial function.
Regulation and function of TRPM7 in human endothelial cells: TRPM7 as a potential novel regulator of endothelial function.
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DOI：
10.1371/journal.pone.0059891
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发表时间：
2013
期刊：
影响因子：
3.7
通讯作者：
Maier JA
中科院分区：
文献类型：
--
作者：
Baldoli E;Castiglioni S;Maier JA
TRPM7是瞬时受体电位通道家族的阳离子通道，已被鉴定为普遍存在的镁转运蛋白。我们在这里表明，TRPM7表达于从脐静脉（HUVEC）分离的内皮细胞，广泛用作大血管内皮模型。静止和衰老不调节TRPM7的量，而通过添加过氧化氢产生的氧化应激增加TRPM7水平。此外，高细胞外镁通过激活钙蛋白酶来降低TRPM 7的水平，而已知促进内皮功能障碍的低细胞外镁部分通过自由基的作用刺激TRPM 7的积累。事实上，抗氧化剂trolox防止TRPM7增加低镁。我们还证明了HUVEC在响应TRPM7的药理学和遗传抑制方面的独特行为，细胞生长和迁移增加。我们的研究结果表明，TRPM7调节内皮细胞的行为，任何条件下导致TRPM7上调可能会损害内皮功能。
TRPM7, a cation channel of the transient receptor potential channel family, has been identified as a ubiquitous magnesium transporter. We here show that TRPM7 is expressed in endothelial cells isolated from the umbilical vein (HUVEC), widely used as a model of macrovascular endothelium. Quiescence and senescence do not modulate TRPM7 amounts, whereas oxidative stress generated by the addition of hydrogen peroxide increases TRPM7 levels. Moreover, high extracellular magnesium decreases the levels of TRPM7 by activating calpains, while low extracellular magnesium, known to promote endothelial dysfunction, stimulates TRPM7 accumulation partly through the action of free radicals. Indeed, the antioxidant trolox prevents TRPM7 increase by low magnesium. We also demonstrate the unique behaviour of HUVEC in responding to pharmacological and genetic inhibition of TRPM7 with an increase of cell growth and migration. Our results indicate that TRPM7 modulates endothelial behavior and that any condition leading to TRPM7 upregulation might impair endothelial function.
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DOI：
10.1073/pnas.1434429100
发表时间：
2003-09-16
影响因子：
11.1
作者：
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通讯作者：
Brown, PO
影响因子：
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作者：
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影响因子：
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影响因子：
6.6
作者：
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影响因子：
6.6
作者：
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