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首页> 外文期刊>Thorax: The Journal of the British Thoracic Society >Acute hypoxia simultaneously induces the expression of gp91phox and endothelial nitric oxide synthase in the porcine pulmonary artery.
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Acute hypoxia simultaneously induces the expression of gp91phox and endothelial nitric oxide synthase in the porcine pulmonary artery.

机译：急性缺氧会同时诱导猪肺动脉中gp91phox和内皮型一氧化氮合酶的表达。

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BACKGROUND: The effect of hypoxia on the formation of superoxide (O(2)(-)), the expression of gp91(phox) and endothelial NO synthase (eNOS) were studied in pig intact pulmonary artery (PA) segments and PA vascular smooth muscle cells (PAVSMCs) and PA endothelial cells (PAECs). METHODS: Segments and cells were incubated under hypoxic conditions for 2 hours (with or without enzyme inhibitors) and the formation of O(2)(-) measured spectrophotometrically. Protein expression was assessed using Western blotting and immunocytochemistry. RESULTS: Hypoxia promoted the formation of O(2)(-) in PA segments, PAVSMCs and PAECs, an effect inhibited by diphenylene iodonium and apocynin (NAD[P]H oxidase inhibitors). Hypoxia induced O(2)(-) formation was enhanced by inhibition of eNOS and augmented by endotoxin and cytokines and re-oxygenation. Hypoxia also promoted the expression of gp91(phox) and eNOS. In intact PA segments hypoxia induced the expression of nitrotyrosine and eNOS in the endothelium. CONCLUSIONS: The simultaneous upregulation of NAD[P]H oxidase and eNOS in response to hypoxia in the PA results in the simultaneous formation of O(2)(-), NO, and ONOO(-). This may represent either a protective mechanism designed to counter the pro-oxidant effect of hypoxia or a novel pathological mechanism underlying the progression of acute respiratory distress syndrome (ARDS).
机译：背景：研究了缺氧对猪完整肺动脉段和PA血管平滑肌中超氧化物（O（2）（-））的形成，gp91（phox）和内皮NO合酶（eNOS）表达的影响。肌肉细胞（PAVSMC）和PA内皮细胞（PAEC）。方法：将片段和细胞在缺氧条件下孵育2小时（有或没有酶抑制剂），并用分光光度法测量O（2）（-）的形成。使用蛋白质印迹和免疫细胞化学评估蛋白质表达。结果：缺氧促进了PA段，PAVSMC和PAEC中O（2）（-）的形成，这种作用被二亚苯基碘鎓和载脂蛋白（NAD [P] H氧化酶抑制剂）抑制。缺氧诱导的O（2）（-）形成通过抑制eNOS增强，并通过内毒素和细胞因子以及再充氧增强。缺氧还促进了gp91（phox）和eNOS的表达。在完整的PA段中，缺氧诱导了内皮中硝基酪氨酸和eNOS的表达。结论：PA缺氧时，NAD [P] H氧化酶和eNOS同时上调导致O（2）（-），NO和ONOO（-）同时形成。这可能代表旨在对抗缺氧的促氧化作用的保护性机制，也可能代表了急性呼吸窘迫综合征（ARDS）进展的新型病理机制。

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