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首页> 外文期刊>Journal of Cellular Physiology >Kir 2.2 inward rectifier potassium channels are inhibited by an endogenous factor in Xenopus oocytes independently from the action of a mitochondrial uncoupler.
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Kir 2.2 inward rectifier potassium channels are inhibited by an endogenous factor in Xenopus oocytes independently from the action of a mitochondrial uncoupler.

机译：吉珥2.2内向整流钾通道被一个非洲爪蟾蜍的内生因素卵母细胞独立的行动线粒体解偶联剂。

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We previously showed inhibition of K(ir)2 inward rectifier K(+) channels expressed in Xenopus oocytes by the mitochondrial agents carbonyl cyanide p-trifluoromethoxyphenylhydrazone (FCCP) and sodium azide. Mutagenesis studies suggested that FCCP may act via phosphatidylinositol 4,5-bisphosphate (PIP(2)) depletion. This mechanism could be reversible in intact cells but not in excised membrane patches which preclude PIP(2) regeneration. This prediction was tested by investigating the reversibility of the inhibition of K(ir)2.2 by FCCP in intact cells and excised patches. We also investigated the effect of FCCP on K(ir)2.2 expressed in human embryonic kidney (HEK) cells. K(ir)2.2 current, expressed in Xenopus oocytes, increased in inside-out patches from FCCP-treated and untreated oocytes. The fraction of total current that increased was 0.79 +/- 0.05 in control and 0.89 +/- 0.03 in 10 microM FCCP-treated (P > .05). Following run-up, oocytes. Therefore, run-up reflected not reversal of inhibition by FCCP,but washout of an endogenous inhibitor. K(ir)2.2 current recovered in intact oocytes within 26.5 h of FCCP removal. Injection of oocytes with 0.1 U apyrase completely depleted ATP (P < .001) but did not inhibit K(ir)2.2 and inhibited K(ir)2.1 by 35% (P < .05). FCCP only partially reduced [ATP] (P < .001), despite inhibiting K(ir)2.2 by 75% (P < .01) but not K(ir)2.1. FCCP inhibited K(ir)2.2 expressed in HEK cells. The recovery of K(ir)2.2 from inhibition by FCCP requires intracellular components, but direct depletion of ATP does not reproduce the differential inhibitory effect of FCCP. Inhibition of K(ir)2.2 by FCCP is not unique to Xenopus oocytes.
机译：我们之前显示抑制内K (ir) 2整流K(+)渠道表达了在非洲爪蟾蜍卵母细胞的线粒体代理羰基氰化物p-trifluoromethoxyphenylhydrazone (FCCP)和叠氮化钠。通过磷脂酰肌醇FCCP可能采取行动4, 5-bisphosphate (PIP)(2)损耗。在完整细胞,但机制可能是可逆的不是掉了膜补丁,排除皮普(2)再生。通过调查的可逆性抑制FCCP 2.2 K (ir)的完整的细胞和切除补丁。FCCP对K的影响(ir) 2.2表达了人类胚胎肾细胞(HEK)。表现在非洲爪蟾蜍卵母细胞增加由内而外从FCCP-treated和补丁未经处理的卵母细胞。增加在控制和0.79 + / - 0.050.89 + / - 0.03在10 microM FCCP-treated (P >. 05)。之前反映不逆转的抑制FCCP,但冲刷的内源性抑制剂。2.2 K (ir)电流恢复完整的卵母细胞在26.5 h FCCP删除。卵母细胞为0.1 U apyrase完全耗尽ATP (P <措施),但没有抑制2.2 K (ir)抑制K (ir) 2.1 35% (P < . 05)。部分(ATP)减少(P <措施),尽管抑制K (ir) 2.2 75% (P < . 01),而不是2.1 K (ir)。HEK细胞。抑制由FCCP需要细胞内组件,但直接消耗ATP并不繁殖的微分的抑制作用FCCP。非洲爪蟾蜍卵母细胞所特有的。

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