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首页> 外文期刊>Pulmonary Circulation >Activity of Ca2+-Activated Cl? Channels Contributes to Regulating Receptor- and Store-Operated Ca2+ Entry in Human Pulmonary Artery Smooth Muscle Cells:
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Activity of Ca2+-Activated Cl? Channels Contributes to Regulating Receptor- and Store-Operated Ca2+ Entry in Human Pulmonary Artery Smooth Muscle Cells:

机译：Ca 2+活化的Cl？通道有助于调节人类肺动脉平滑肌细胞中受体和储存操作的Ca2 +进入：

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Intracellular Ca2+ plays a fundamental role in regulating cell functions in pulmonary arterial smooth muscle cells (PASMCs). A rise in cytosolic Ca2+ concentration ([Ca2+]cyt) triggers pulmonary vasoconstriction and stimulates PASMC proliferation. [Ca2+]cyt is increased mainly by Ca2+ release from intracellular stores and Ca2+ influx through plasmalemmal Ca2+-permeable channels. Given the high concentration of intracellular Cl? in PASMCs, Ca2+-activated Cl? (ClCa) channels play an important role in regulating membrane potential and cell excitability of PASMCs. In this study, we examined whether activity of ClCa channels was involved in regulating [Ca2+]cyt in human PASMCs via regulating receptor- (ROCE) and store- (SOCE) operated Ca2+ entry. The data demonstrated that an angiotensin II (100 nM)-mediated increase in [Ca2+]cyt via ROCE was markedly attenuated by the ClCa channel inhibitors, niflumic acid (100 μM), flufenamic acid (100 μM), and 4,4′-diisothiocyanatostilbene-2,2′-disulfonic acid (100 μM). The inhibition of ClCa channels by niflumic acid and flufenamic acid significantly reduced both transient and plateau phases of SOCE that was induced by passive depletion of Ca2+ from the sarcoplasmic reticulum by 10 μM cyclopiazonic acid. In addition, ROCE and SOCE were abolished by SKF-96365 (50 μM) and 2-aminoethyl diphenylborinate (100 μM), and were slightly decreased in the presence of diltiazem (10 μM). The electrophysiological and immunocytochemical data indicate that ClCa currents were present and TMEM16A was functionally expressed in human PASMCs. The results from this study suggest that the function of ClCa channels, potentially formed by TMEM16A proteins, contributes to regulating [Ca2+]cyt by affecting ROCE and SOCE in human PASMCs.
机译：细胞内Ca2 +在调节肺动脉平滑肌细胞（PASMC）的细胞功能中起着基本作用。胞质Ca2 +浓度（[Ca2 +] cyt）升高会触发肺血管收缩并刺激PASMC增殖。 [Ca2 +] cyt的增加主要是由于细胞内存储中的Ca2 +释放以及通过血浆Ca2 +渗透通道的Ca2 +流入。鉴于细胞内Cl 2浓度高。在PASMC中，Ca2 +激活的Cl？ （ClCa）通道在调节PASMC的膜电位和细胞兴奋性中起重要作用。在这项研究中，我们检查了ClCa通道的活性是否通过调节受体-（ROCE）和贮存-（SOCE）操纵的Ca2 +进入来参与调节人PASMC中的[Ca2 +] cyt。数据表明，ClCa通道抑制剂，尼氟酸（100μM），氟苯那酸（100μM）和4,4'-明显抑制了血管紧张素II（100 nM）通过ROCE介导的[Ca2 +] cyt的增加。 diisothiocyanatostilbene-2,2'-disulfonic acid（100μM）。烟酰胺酸和氟草酸抑制ClCa通道可显着降低SOCE的瞬态和平稳相，这是由10μM环吡嗪酸从肌质网被动消耗Ca2 +诱导的。此外，SKF-96365（50μM）和2-氨基乙基二苯基硼酸酯（100μM）废除了ROCE和SOCE，并且在地尔硫卓（10μM）存在下略有降低。电生理和免疫细胞化学数据表明，在人PASMC中存在ClCa电流并且TMEM16A在功能上表达。这项研究的结果表明，可能由TMEM16A蛋白形成的ClCa通道功能通过影响人类PASMCs的ROCE和SOCE有助于调节[Ca2 +] cyt。

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