TRPC3 participates in angiotensin II type 1 receptor-dependent stress-induced slow increase in intracellular Ca2+ concentration in mouse cardiomyocytes
TRPC3 participates in angiotensin II type 1 receptor-dependent stress-induced slow increase in intracellular Ca2+ concentration in mouse cardiomyocytes
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TRPC3参与血管紧张素II 1型受体依赖性应激诱导的小鼠心肌细胞内Ca2+浓度缓慢增加
DOI：
10.1007/s12576-016-0519-3
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发表时间：
2017
期刊：
影响因子：
--
通讯作者：
Naruse K.
中科院分区：
文献类型：
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作者：
Yamaguchi Y;Iribe G;Kaneko T;Takahashi K;Numaga-Tomita T;Nishida M;Birnbaumer L;Naruse K.
当心肌处于拉伸位置时，其[Ca2+]瞬态在几分钟内缓慢增加，这一过程被称为应力诱导的细胞内Ca2+浓度缓慢增加（[Ca2+]i） （SSC）。瞬时受体电位规范（TRPC） 3形成由血管紧张素II 1型受体（AT1R）调节的非选择性阳离子通道。在这项研究中，我们研究了TRPC3在SSC中的作用。电刺激分离的小鼠心室肌细胞并使其持续拉伸。AT1R阻滞剂、磷脂酶C抑制剂和TRPC3抑制剂抑制SSC。这些抑制剂还消除了血管紧张素II诱导的ssc样的[Ca2+]i缓慢增加，而不是拉伸。此外，在TRPC3敲除小鼠中未观察到SSC。模拟和免疫组织化学研究表明，肌上皮TRPC3与SSC有关。这些结果表明，由AT1R调控的肌层TRPC3可引起SSC。
When a cardiac muscle is held in a stretched position, its [Ca2+] transient increases slowly over several minutes in a process known as stress-induced slow increase in intracellular Ca2+concentration ([Ca2+]i) (SSC). Transient receptor potential canonical (TRPC) 3 forms a non-selective cation channel regulated by the angiotensin II type 1 receptor (AT1R). In this study, we investigated the role of TRPC3 in the SSC. Isolated mouse ventricular myocytes were electrically stimulated and subjected to sustained stretch. An AT1R blocker, a phospholipase C inhibitor, and a TRPC3 inhibitor suppressed the SSC. These inhibitors also abolished the observed SSC-like slow increase in [Ca2+]iinduced by angiotensin II, instead of stretch. Furthermore, the SSC was not observed in TRPC3 knockout mice. Simulation and immunohistochemical studies suggest that sarcolemmal TRPC3 is responsible for the SSC. These results indicate that sarcolemmal TRPC3, regulated by AT1R, causes the SSC.