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首页> 外文期刊>Life sciences >15-Hydroxyeicosatetraenoic acid (15-HETE) protects pulmonary artery smooth muscle cells against apoptosis via HSP90.
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15-Hydroxyeicosatetraenoic acid (15-HETE) protects pulmonary artery smooth muscle cells against apoptosis via HSP90.

机译：15-Hydroroxyeicosatetraenoic酸（15-HETE）通过HSP90保护肺动脉平滑肌细胞免于凋亡。

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摘要

AIMS: 15-Hydroxyeicosatetraenoic acid (15-HETE), generated by hypoxia, is a product of arachidonic acid and mainly catalyzed by 15-lipoxygenase (15-LO) in pulmonary artery. As HSP90 is known to be involved in apoptosis in other tissues and cells, we aim to test whether anti-apoptotic effect of 15-HETE is regulated by the molecular chaperone in pulmonary artery smooth muscle cells. MAIN METHODS: To test this hypothesis, we performed cell viability analysis, mitochondrial potential assay, caspase-3 activity measurement, Western blot, and terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling with and without HSP90 inhibitor. KEY FINDINGS: Our results showed that both exogenous and endogenous 15-HETE up-regulated HSP90 expression and prevented PASMC from serum deprivation-induced apoptosis. Serum deprivation lead to mitochondrial membrane depolarization, decreased expression of Bcl-2 and enhanced expression of Bax, and activation of caspase-3 and caspase-9 in PASMCs. 15-HETE reversed all these effects in a HSP90-dependent manner. SIGNIFICANCE: This study establishes the factor involved in 15-HETE-protecting PASMC from apoptosis and the regulation of HSP90 by 15-HETE may be an important mechanism underlying the treatment of pulmonary artery hypertension and provide a novel therapeutic target in future.
机译：目的：由缺氧产生的15-羟基二十二碳四烯酸（15-HETE）是花生四烯酸的产物，主要由肺动脉中的15-脂氧合酶（15-LO）催化。由于已知HSP90参与其他组织和细胞的凋亡，因此我们旨在测试15-HETE的抗凋亡作用是否受分子伴侣在肺动脉平滑肌细胞中的调节。主要方法：为了验证该假设，我们进行了细胞生存力分析，线粒体电位测定，caspase-3活性测定，蛋白质印迹和带有和不带有HSP90抑制剂的末端脱氧核苷酸转移酶介导的dUTP缺口末端标记。关键发现：我们的结果表明，外源性和内源性15-HETE均可上调HSP90表达，并阻止PASMC发生血清剥夺诱导的细胞凋亡。血清剥夺导致PASMCs线粒体膜去极化，Bcl-2表达降低和Bax表达增强以及caspase-3和caspase-9活化。 15-HETE以依赖HSP90的方式逆转了所有这些作用。意义：这项研究建立了参与15-HETE保护PASMC凋亡的因素，而15-HETE对HSP90的调节可能是治疗肺动脉高压的重要机制，并在将来提供了新的治疗靶标。

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