首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >B2 receptor activation reduces Erk1 and Erk2 phosphorylation induced by insulin-like growth factor-1, platelet-derived growth factor-BB, and high glucose in rat isolated glomeruli.
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B2 receptor activation reduces Erk1 and Erk2 phosphorylation induced by insulin-like growth factor-1, platelet-derived growth factor-BB, and high glucose in rat isolated glomeruli.

机译:B2受体激活减少了大鼠分离的肾小球中胰岛素样生长因子-1,血小板衍生的生长因子-BB和高糖诱导的Erk1和Erk2磷酸化。

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摘要

Several experimental data document an activation of the mitogen-activated protein kinases Erk1 and Erk2 by bradykinin (BK), an agonist of the kinin B2 receptor (B2R). In contrast, other reports showed an inhibitory modulation of mitogenesis by BK. Therefore, we explored in the isolated glomeruli the effect of B2R activation on the signaling of insulin-like growth factor-1 (IGF-1), platelet-derived growth factor-BB (PDGF-BB), and high glucose (HG), three factors that are believed to be involved in the development of glomerulosclerosis via the phosphorylation of Erk1 and Erk2. We observed that the activation of B2R negatively modulates the phosphorylation of Erk1 and Erk2 induced by IGF-1, PDGF-BB, and HG in the glomerulus. These effects are consistent with the hypothesis of a protective role for BK in the kidney during development of glomerulosclerosis and renal pathologies associated with a hyperproliferative state.
机译:一些实验数据记录了激肽B2受体(B2R)的激动剂缓激肽(BK)对丝裂原激活的蛋白激酶Erk1和Erk2的激活。相反,其他报道显示BK抑制有丝分裂发生。因此,我们在离体的肾小球中探索了B2R激活对胰岛素样生长因子1(IGF-1),血小板衍生生长因子BB(PDGF-BB)和高血糖(HG)信号传导的影响,通过Erk1和Erk2的磷酸化,三个因素被认为与肾小球硬化的发展有关。我们观察到,B2R的激活对肾小球中IGF-1,PDGF-BB和HG诱导的Erk1和Erk2的磷酸化产生负调控。这些作用与在肾小球硬化和与过度增殖状态相关的肾脏病理发展过程中BK在肾脏中具有保护作用的假设相一致。

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