Crosstalk between protective autophagy and NF-κB signal in high glucose-induced podocytes

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• 作者：Miaomiao Wei (1)
  Zhigui Li (1)
  Zhuo Yang (1)
  
• 关键词：Nuclear factor ; kappa B ; Autophagy ; Apoptosis ; Podocytes ; High glucose
• 刊名：Molecular and Cellular Biochemistry
• 出版年：2014
• 出版时间：September 2014
• 年：2014
• 卷：394
• 期：1-2
• 页码：261-273
• 全文大小：9,039 KB
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• 作者单位：Miaomiao Wei (1)
  Zhigui Li (1)
  Zhuo Yang (1)
  
  1. College of Medicine, Tianjin Key Laboratory of Tumor Microenvironment and Neurovascular Regulation, State Key Laboratory of Medicinal Chemical Biology, Nankai University, Tianjin, 300071, China
  
• ISSN：1573-4919

文摘

Despite a great deal of recent studies focused on the pivotal role of autophagy in maintaining podocyte energy homeostasis, the mechanisms of autophagy in regulating transcriptional factors under high glucose (HG) condition are not fully understood. Here, we evaluated the effect of HG on nuclear factor-kappa B (NF-κB) signaling and autophagic process. The results showed that HG promoted autophagy in podocytes. Bafilomycin A1 (Baf A1) further enhanced this effect, but 3-methyadenine (3-MA) inhibited it. The proautophagic effects of HG manifested in the form of enhanced podocyte expression of light chain 3 (LC3)-II. In these cells, blockade of NF-κB signal by ammonium pyrrolidinethiocarbamate constrained in effectively reducing LC3-II up-regulation and increasing podocyte apoptosis. Furthermore, the autophagy inhibitors, such as Baf A1 and 3-MA, significantly enhanced HG-induced NF-κB activation and increased apoptosis. Thus, we conclude that the accumulation of autophagosomes results from enhancement of the autophagic flux, but not the blockage of autophagosome–lysosome fusion by HG. We also prove that HG-induced apoptosis, autophagy, and NF-κB signal are in a close crosstalk through a yet undetermined mechanism in podocytes.