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首页> 外文期刊>American Journal of Physiology >Cytosolic NADH redox and thiol oxidation regulate pulmonary arterial force through ERK MAP kinase.
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Cytosolic NADH redox and thiol oxidation regulate pulmonary arterial force through ERK MAP kinase.

机译：胞质NADH氧化还原和硫醇氧化通过ERK MAP激酶调节肺动脉力量。

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An ERK MAP kinase-mediated contractile mechanism previously reported to be activated by peroxide and stretch in bovine coronary arteries is shown in this study to be present in endothelium-denuded bovine pulmonary arteries and subject to regulation by modulation of cytosolic NAD(H) redox through the lactate dehydrogenase reaction. Although our previous work identified an acute PO2-dependent peroxide-mediated relaxation of bovine pulmonary arteries on exposure to lactate, a 30-min treatment with 10 mM lactate enhanced ERK phosphorylation and increased force generation to 30 mM KCl. Hypoxia inhibited these responses to lactate. Increases in ERK phosphorylation and the enhancement of force generation by lactate and stretch are attenuated in the presence of inhibitors of Nox oxidase (0.1 mM apocynin) or ERK activation (10 microM PD-98059) and by 0.1 mM ebselen. Additionally, incubation of pulmonary arteries with 10 mM pyruvate lowered basal levels of ERK phosphorylation, and it inhibited both the ERK phosphorylation and the enhancement in force generation to 30 mM KCl caused by stretch. Treatment of pulmonary arteries with the thiol oxidant diamide (1 microM) elicited what appears to be a peroxide-independent increase in force and ERK phosphorylation that were both attenuated by PD-98059. Thus pulmonary arteries possess a peroxide-elicited contractile mechanism involving ERK MAP kinase, which is stimulated by stretch and regulated through the control of Nox oxidase activity by the availability of cytosolic NADH.
机译：这项研究表明，ERK MAP激酶介导的收缩机制先前已被过氧化物激活并在牛冠状动脉中拉伸。该研究显示该物质存在于内皮剥脱的牛肺动脉中，并通过调节细胞质中的NAD（H）氧化还原而受到调节。乳酸脱氢酶反应。尽管我们先前的工作发现暴露于乳酸中后牛肺动脉具有PO2依赖性的过氧化物介导的急性舒张作用，但用10 mM乳酸进行的30分钟处理可增强ERK磷酸化，并增加产生力至30 mM KCl。低氧抑制了这些对乳酸的反应。在存在Nox氧化酶（0.1 mM阿朴西宁）或ERK激活（10 microM PD-98059）和0.1 mM依布硒啉的抑制剂的存在下，ERK磷酸化的增加以及乳酸和拉伸产生的力的增强被减弱。此外，用10 mM丙酮酸孵育肺动脉降低了基础水平的ERK磷酸化，并且抑制了ERK磷酸化，并抑制了由拉伸引起的力量增强至30 mM KCl。用硫醇氧化剂二酰胺（1 microM）治疗肺动脉引起似乎独立于过氧化物的作用力增加和ERK磷酸化，两者均被PD-98059减弱。因此，肺动脉具有涉及ERK MAP激酶的过氧化物引发的收缩机制，该机制受牵张刺激并通过胞质NADH的有效利用来控制Nox氧化酶的活性。

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