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首页> 外文期刊>Cell biology international. >Role of PKCζ‐NADPH oxidase signaling axis in PKCα‐mediated Giα2 phosphorylation for inhibition of adenylate cyclase activity by angiotensin II in pulmonary artery smooth muscle cells
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Role of PKCζ‐NADPH oxidase signaling axis in PKCα‐mediated Giα2 phosphorylation for inhibition of adenylate cyclase activity by angiotensin II in pulmonary artery smooth muscle cells

机译：PKCζ-NADPH氧化酶信号轴在PKCα介导的Giα2磷酸化中的作用，用于抑制血管紧张素II在肺动脉平滑肌细胞中血管紧张素环酶活性的磷酸盐

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Abstract We sought to determine the mechanism by which angiotensin II (AngII) inhibits isoproterenol induced increase in adenylate cyclase (AC) activity and cyclic adenosine monophosphate (cAMP) production in bovine pulmonary artery smooth muscle cells (BPASMCs). Treatment with AngII stimulates protein kinase C‐ζ (PKC‐ζ), nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, and PKC‐α activities, and also inhibits isoproterenol induced increase in AC activity and cAMP production in the cells. Pertussis toxin pretreatment eliminates AngII caused inhibition of isoproterenol induced increase in AC activity without a discernible change in PKC‐ζ, NADPH oxidase, and PKC‐α activities. Treatment of the cells with AngII increases α2 isoform of Gi (Giα2) phosphorylation; while pretreatment with chemical and genetic inhibitors of PKC‐ζ and NADPH oxidase attenuate AngII induced increase in PKC‐α activity and Giα2 phosphorylation, and also reverse AngII caused inhibition of isoproterenol induced increase in AC activity. Pretreatment of the cells with chemical and genetic inhibitors of PKC‐α attenuate AngII induced increase in Giα2 phosphorylation and inhibits isoproterenol induced increase in AC activity without a discernible change in PKC‐ζ and NADPH oxidase activities. Overall, PKCζ‐NADPH oxidase‐PKCα signaling axis plays a crucial role in Giα2 phosphorylation resulting in AngII‐mediated inhibition of isoproterenol induced increase in AC activity in BPASMCs.
机译：我们试图确定血管紧张素II（AngII）抑制异丙肾上腺素诱导的牛肺动脉平滑肌细胞（BPASMC）腺苷酸环化酶（AC）活性和环磷酸腺苷（cAMP）生成的机制。用AngII治疗可刺激蛋白激酶C‐ζ（PKC‐ζ）、烟酰胺腺嘌呤二核苷酸磷酸（NADPH）氧化酶和PKC‐α活性，还可抑制异丙肾上腺素诱导的细胞AC活性增加和cAMP生成。百日咳毒素预处理消除了AngII对异丙肾上腺素诱导的AC活性增加的抑制作用，而PKCζ、NADPH氧化酶和PKCα活性没有明显变化。用AngII处理细胞可增加Gi（Giα2）磷酸化的α2亚型；而用PKCζ和NADPH氧化酶的化学和遗传抑制剂预处理可以减弱AngII诱导的PKCα活性和Giα2磷酸化的增加，也可以逆转AngII对异丙肾上腺素诱导的AC活性增加的抑制。用PKC-α的化学和遗传抑制剂预处理细胞可减弱AngII诱导的Giα2磷酸化增加，并抑制异丙肾上腺素诱导的AC活性增加，而PKC-ζ和NADPH氧化酶活性无明显变化。总之，PKCζ-NADPH氧化酶-PKCα信号轴在Giα2磷酸化中起着关键作用，导致AngII介导的对异丙肾上腺素诱导的BPASMC AC活性增加的抑制。

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