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首页> 外文期刊>Cellular Physiology and Biochemistry >Hypoxia inducible factor-1 improves the actions of nitric oxide and natriuretic peptides after simulated ischemia-reperfusion
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Hypoxia inducible factor-1 improves the actions of nitric oxide and natriuretic peptides after simulated ischemia-reperfusion

机译：缺氧诱导因子-1改善模拟缺血再灌注后一氧化氮和利钠肽的作用

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Ischemia-reperfusion reduces the negative functional effects of cyclic GMP in cardiac myocytes. In this study, we tested the hypothesis that upregulation of hypoxic inducible factor-1 (HIF-1) would improve the actions of cyclic GMP signaling following simulated ischemia-reperfusion. HIF-1 alpha was increased with deferoxamine (150 mg/kg for 2 days). Rabbit cardiac myocytes were subjected to simulated ischemia [15 min 95% N-2-5% CO2] and reperfusion [reoxygenation] to produce myocyte stunning. Cell function was measured utilizing a video-edge detector. Shortening was examined at baseline and after brain natriuretic peptide (BNP, 10(-8), 10(-7)M) or S-nitroso-N-acetyl-penicillamine (SNAP, 10(-6), 10(-5)M) followed by KT5823 (cyclic GMP protein kinase inhibitor, 10(-6)M). Kinase activity was measured via a protein phosphorylation assay. Under control conditions, BNP (-30%) and SNAP (-41%) reduced percent shortening, while KT5823 partially restored function (+18%). Deferoxamine treated control myocytes responded similarly. In stunned myocytes, BNP (-21%) and SNAP (-25%) reduced shortening less and KT5823 did not increase function (+2%). Deferoxamine increased the effects of BNP (-38%) and SNAP (-41%) in stunning and restored the effects of KT5823 (+12%). The cyclic GMP protein kinase increased phosphorylation of several proteins in control HIF-1 +/- cells. Phosphorylation was reduced in stunned cells and was restored in deferoxamine treated stunned cells. This study demonstrated that simulated ischemia-reperfusion reduced the negative functional effects of increasing cyclic GMP and this was related to reduced effects of the cyclic GMP protein kinase. Increased HIF-1 alpha protects the functional effects of cyclic GMP thorough maintenance of cyclic GMP protein kinase activity after ischemic-reperfusion.
机译：缺血再灌注减少了心肌细胞中循环GMP的负面功能。在这项研究中，我们测试了以下假设：缺氧诱导因子-1（HIF-1）的上调将改善模拟缺血再灌注后循环GMP信号的作用。用去铁胺（150 mg / kg持续2天）增加HIF-1α。对兔心肌细胞进行模拟缺血[15分钟，95％N-2-5％CO2]，然后再灌注[复氧]，以产生心肌细胞骤冷。利用视频边缘检测器测量细胞功能。在基线和脑钠肽（BNP，10（-8），10（-7）M）或S-亚硝基-N-乙酰青霉胺（SNAP，10（-6），10（-5）之后检查缩短M），然后是KT5823（环状GMP蛋白激酶抑制剂，10（-6）M）。激酶活性通过蛋白质磷酸化测定来测量。在控制条件下，BNP（-30％）和SNAP（-41％）减少了缩短的百分数，而KT5823部分恢复了功能（+ 18％）。去铁胺处理的对照肌细胞反应相似。在震惊的心肌细胞中，BNP（-21％）和SNAP（-25％）减少的缩短时间减少，而KT5823并未增加功能（+ 2％）。去铁胺提高了BNP（-38％）和SNAP（-41％）的惊醒效果，并恢复了KT5823（+ 12％）的效果。环状GMP蛋白激酶可增强对照HIF-1 +/-细胞中几种蛋白质的磷酸化。磷酸化在被击晕的细胞中减少，并在去铁胺处理的被击晕的细胞中恢复。这项研究表明，模拟的局部缺血-再灌注减少了环状GMP增加的负面功能影响，这与环状GMP蛋白激酶的作用减少有关。缺血再灌注后，HIF-1α的增加可通过完全维持环状GMP蛋白激酶活性来保护环状GMP的功能作用。

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