Hydrogen sulfide and hypoxia-induced changes in TASK (K2P3/9) activity and intracellular Ca(2+) concentration in rat carotid body glomus cells.
Hydrogen sulfide and hypoxia-induced changes in TASK (K2P3/9) activity and intracellular Ca(2+) concentration in rat carotid body glomus cells.
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DOI：
10.1016/j.resp.2015.04.012
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发表时间：
2015-08-15
影响因子：
2.3
通讯作者：
Carroll JL
中科院分区：
文献类型：
--
作者：
Kim D;Kim I;Wang J;White C;Carroll JL
急性缺氧使颈动脉体化学感受器（glomus）细胞去极化并升高细胞内Ca 2+浓度（[Ca 2 +]i）。最近的研究表明，硫化氢（H2S）可能作为一个氧传感器/信号在颈动脉体在急性缺氧。为了进一步测试H2S的这种作用，我们研究了H2S对ASK通道活性和[Ca 2 +]i的影响，这被认为是介导血管球细胞对缺氧的反应的重要因素。与缺氧一样，NaHS（H2S供体）抑制了ASK活性并升高了[Ca 2 +]i。为了抑制H2S的产生，将血管球细胞与胱硫醚-β-合酶和胱硫醚-γ-裂解酶的抑制剂（DL-炔丙基甘氨酸、氨氧基乙酸、β-氰基-L-丙氨酸; 0.3 mM）孵育（3 hr）。SF 7荧光用于评估H2S产生的水平。抑制剂阻断L-半胱氨酸和缺氧诱导的SF 7荧光强度升高。在用抑制剂处理的细胞中，缺氧产生了对ASK活性的抑制和[Ca 2 +]i的升高，其幅度与在对照细胞中观察到的相似。L-半胱氨酸对ASK活性和[Ca ~（2+）]i无影响，也不影响缺氧诱导的ASK抑制和[Ca ~（2+）]i升高。这些结果表明，在正常条件下，H2S不是缺氧诱导的ASK通道和[Ca 2 +]i在分离的血管球细胞的调制的主要信号。
Acute hypoxia depolarizes carotid body chemoreceptor (glomus) cells and elevates intracellular Ca2+ concentration ([Ca2+]i). Recent studies suggest that hydrogen sulfide (H2S) may serve as an oxygen sensor/signal in the carotid body during acute hypoxia. To further test such a role for H2S, we studied the effects of H2S on the activity of TASK channel and [Ca2+]i, which are considered important for mediating the glomus cell response to hypoxia. Like hypoxia, NaHS (a H2S donor) inhibited TASK activity and elevated [Ca2+]i. To inhibit the production of H2S, glomus cells were incubated (3 hr) with inhibitors of cystathionine-β-synthase and cystathionine-γ-lyase (DL-propargylglycine, aminooxyacetic acid, β-cyano-L-alanine; 0.3 mM). SF7 fluorescence was used to assess the level of H2S production. The inhibitors blocked L-cysteine- and hypoxia-induced elevation of SF7 fluorescence intensity. In cells treated with the inhibitors, hypoxia produced an inhibition of TASK activity and a rise in [Ca2+]i, similar in magnitude to those observed in control cells. L-cysteine produced no effect on TASK activity or [Ca2+]i and did not affect hypoxia-induced inhibition of TASK and elevation of [Ca2+]i. These findings suggest that under normal conditions, H2S is not a major signal in hypoxia-induced modulation of TASK channels and [Ca2+]i in isolated glomus cells.
影响因子：
5.3
作者：
Otsubo T;Kostuk EW;Balbir A;Fujii K;Shirahata M
通讯作者：
Shirahata M