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首页> 外文期刊>American Journal of Physiology >ANG II promotes autophagy in podocytes.
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ANG II promotes autophagy in podocytes.

机译：ANG II促进足细胞自噬。

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Podocytes are an integral and important constituent of the glomerular filtration barrier (GFB) and are exposed to a higher concentrations of ANG II in diseased states; consequently, podocytes may accumulate oxidized proteins and damaged mitochondria. In the present study, we evaluated the effect of ANG II on the podocyte autophagic process, which is likely to be triggered in order to degrade unwanted proteins and damaged organelles. To quantitate the occurrence of autophagy, electron microscopic studies were carried out on control and ANG II-treated conditionally immortalized mouse podocytes (CIMPs). ANG II-treated cells showed a fivefold greater number of autophagosomes/field compared with control cells. This proautophagic effect of ANG II was inhibited by pretreatment with 3-methyladenine, an inhibitor of autophagy. ANG II also enhanced podocyte expression of autophagic genes such as LC3-2 and beclin-1. Since oxidative stress is often associated with the induction of autophagy, we examined the effect of ANG II on podocyte reactive oxygen species (ROS) generation. ANG II enhanced podocyte ROS generation in a time-dependent manner. To determine whether there is a causal relationship between ANG II-induced oxidative stress and induction of autophagy, we evaluated the effect of antioxidants on ANG II-induced autophagy. As expected, the proautophagic effect of ANG II was inhibited by antioxidants. We conclude that ANG II promotes podocyte autophagy through the generation of ROS.
机译：足细胞是肾小球滤过屏障（GFB）不可或缺的重要组成部分，在患病状态下会暴露于较高浓度的ANG II。因此，足细胞可能积聚氧化蛋白质和受损的线粒体。在本研究中，我们评估了ANG II对足细胞自噬过程的影响，这可能是为了降解不需要的蛋白质和受损的细胞器而触发的。为了定量自噬的发生，对对照和ANG II处理的条件永生小鼠足细胞（CIMP）进行了电子显微镜研究。与对照细胞相比，ANG II处理的细胞显示自噬体/视野的数量大五倍。通过用3-甲基腺嘌呤（一种自噬抑制剂）进行预处理，可以抑制ANG II的这种自噬作用。 ANG II还增强了自噬基因如LC3-2和beclin-1的足细胞表达。由于氧化应激通常与自噬的诱导有关，因此我们检查了ANG II对足细胞活性氧（ROS）生成的影响。 ANG II以时间依赖性方式增强足细胞ROS的产生。为了确定ANG II诱导的氧化应激与自噬诱导之间是否存在因果关系，我们评估了抗氧化剂对ANG II诱导的自噬的影响。如预期的那样，抗氧化剂抑制了ANG II的自噬作用。我们得出结论，ANG II通过产生ROS促进足细胞自噬。

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