Autophagy protects podocytes from sublytic complement induced injury
Autophagy protects podocytes from sublytic complement induced injury
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DOI：
10.1016/j.yexcr.2016.02.009
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发表时间：
2016-02-15
影响因子：
3.7
通讯作者：
Zhang, Yu
中科院分区：
文献类型：
--
作者：
Lv, Qianying;Yang, Fengjie;Zhang, Yu
补体亚溶解攻击引起足细胞损伤是膜性肾病的主要特征。本研究旨在探讨亚溶解性补体攻击相关的自噬对体外足细胞损伤的影响。在这里，我们表明，亚裂解补体攻击增强MPC 5足细胞自噬体外。用3-甲基腺嘌呤（3-MA）治疗抑制自噬显著增加了亚溶解性补体攻击诱导的损伤相关形态学、应力纤维和足细胞凋亡的变化，但降低了MPC 5足细胞的存活和粘附。相比之下，促进自噬治疗雷帕霉素减轻亚溶解补体攻击诱导的损伤相关的形态学，应力纤维和足细胞凋亡的变化，但增加了MPC 5足细胞的存活和粘附。这些数据表明，自噬可以保护足细胞免受亚溶解性补体攻击诱导的体外损伤。(C)2016 Elsevier Inc. All rights reserved.
Podocyte injury induced by sublytic complement attack is the main feature of membranous nephropathy (MN). This study aimed at investigating the impact of sublytic complement attack-related autophagy on podocyte injury in vitro. Here, we show that sublytic complement attack enhances MPC5 podocyte autophagy in vitro. Inhibition of autophagy by treatment with 3-methyladenine (3-MA) significantly increased sublytic complement attack-induced changes in the injury-related morphology, stress fiber, and podocyte apoptosis, but decreased the survival and adhesion of MPC5 podocytes. In contrast, promotion of autophagy by treatment with rapamycin mitigated sublytic complement attack-induced changes in the injury-related morphology, stress fiber, and podocyte apoptosis, but increased the survival and adhesion of MPC5 podocytes. These data suggest that autophagy may protect podocytes from sublytic complement attack-induced injury in vitro. (C) 2016 Elsevier Inc. All rights reserved.