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首页> 外文期刊>Life sciences >Differential roles of MAP kinases in atorvastatin-induced VEGF release in cardiac myocytes.
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Differential roles of MAP kinases in atorvastatin-induced VEGF release in cardiac myocytes.

机译：MAP激酶在阿托伐他汀诱导的心肌细胞VEGF释放中的不同作用。

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Statins, specific inhibitors of 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase, are now widely used for treatment of patients with hypercholesterolemia. In addition to the reduction of cholesterol biosynthesis, accumulating evidence indicates that statins have several pleiotropic effects especially on cardiovascular system. However, the exact role of statin in cardiac myocytes remains unclear. In the present study, we investigated whether atorvastatin induces vascular endothelial growth factor (VEGF) release in cardiac myocytes, and the underlying mechanism. We observed that atorvastatin significantly stimulated VEGF release in a dose-dependent manner. It induced the phosphorylation of p44/p42 mitogen-activated protein (MAP) kinase and p38 MAP kinase but not SAPK (stress-activated protein kinase)/JNK (c-Jun N-terminal kinase). The atorvastatin-induced VEGF release was enhanced by PD98059, which is a specific inhibitor of the upstream kinase that activates p44/p42 MAP kinase (MEK). Further, it was significantly reduced by SB203580, a specific inhibitor of p38 MAP kinase. Furthermore, the atorvastatin-induced phosphorylation of p38 MAP kinase was attenuated by SB203580, whereas it was enhanced by PD98059. Taken together, these results suggest that the atorvastatin-induced VEGF release in cardiac myocytes is positively regulated by p38 MAP kinase and negatively regulated byp44/p42 MAP kinase and that the atorvastatin-induced phosphorylation of p38 MAP kinase is regulated by p44/p42 MAP kinase in these cells.
机译：他汀类药物是3-羟基-3-甲基戊二酰辅酶A（HMG-CoA）还原酶的特异性抑制剂，现已广泛用于治疗高胆固醇血症患者。除了减少胆固醇的生物合成外，越来越多的证据表明他汀类药物具有多种功效，尤其是对心血管系统。然而，他汀类药物在心肌细胞中的确切作用仍不清楚。在本研究中，我们调查了阿托伐他汀是否诱导心肌细胞中的血管内皮生长因子（VEGF）释放及其潜在机制。我们观察到阿托伐他汀以剂量依赖性方式显着刺激VEGF释放。它诱导了p44 / p42丝裂原活化蛋白（MAP）激酶和p38 MAP激酶的磷酸化，但不诱导SAPK（应激活化蛋白激酶）/ JNK（c-Jun N-末端激酶）。 PD98059可增强阿托伐他汀诱导的VEGF释放，PD98059是激活p44 / p42 MAP激酶（MEK）的上游激酶的特异性抑制剂。此外，它被p38 MAP激酶的特异性抑制剂SB203580显着降低。此外，SB203580减弱了阿托伐他汀诱导的p38 MAP激酶的磷酸化，而PD98059增强了磷酸化。综上所述，这些结果表明，阿托伐他汀诱导的心肌细胞中的VEGF释放受p38 MAP激酶正调控，而受p44 / p42 MAP激酶负调控，而阿托伐他汀诱导的p38 MAP激酶磷酸化受p44 / p42 MAP激酶调控。在这些细胞中。

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