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首页> 外文期刊>American Journal of Physiology >Potential role of cartilage oligomeric matrix protein in the modulation of pulmonary arterial smooth muscle superoxide by hypoxia
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Potential role of cartilage oligomeric matrix protein in the modulation of pulmonary arterial smooth muscle superoxide by hypoxia

机译:软骨寡聚基质蛋白在缺氧调节肺动脉平滑肌超氧化物中的潜在作用

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摘要

Changes in reactive oxygen species and extracellular matrix seem to participate in pulmonary hypertension development. Because we recently reported evidence for chronic hypoxia decreasing expression of cartilage oligomeric matrix protein (COMP) and evidence for this controlling loss of pulmonary arterial smooth muscle bone morpho-genetic protein receptor-2 (BMPR2) and contractile phenotype proteins, we examined if changes in superoxide metabolism could be an important factor in a bovine pulmonary artery (BPA), organoid cultured under hypoxia for 48 h model. Hypoxia (3% O_2) caused a depletion of COMP in BPA, but not in bovine coronary arteries. Knockdown of COMP by small-interfering RNA (siRNA) increased BPA levels of mitochondrial and extra-mitochondria] superoxide detected by MitoSOX and dihydroethidium (DHE) HPLC products.
机译:活性氧物质和细胞外基质的变化似乎参与了肺动脉高压发育。 因为我们最近报告了慢性缺氧的证据降低了软骨寡聚基蛋白(COMP)的表达和这种控制肺动脉平滑肌骨质遗传蛋白受体-2(BMPR2)和收缩表型蛋白的证据,我们检查了变化 超氧化酯代谢可能是牛肺动脉(BPA)的重要因素,在缺氧下培养48小时模型。 缺氧(3%O_2)引起BPA中的COMP耗尽,但不含牛冠状动脉。 通过小干扰RNA(siRNA)敲低COMP的BPA水平的线粒体和超细色素的水平,MitoSox和二氢丙酮(DHE)HPLC产物检测到的超氧化物。

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