High glucose induces autophagy in podocytes

被引:115
作者
Ma, Tean [1 ]
Zhu, Jili [1 ]
Chen, Xinghua [1 ]
Zha, Dongqing [1 ]
Singhal, Pravin C. [2 ]
Ding, Guohua [1 ]
机构
[1] Wuhan Univ, Renmin Hosp, Div Nephrol, Wuhan 430060, Hubei, Peoples R China
[2] North Shore LIJ Hlth Syst, Div Kidney Dis & Hypertens, Great Neck, NY 11021 USA
基金
美国国家科学基金会;
关键词
Autophagy; High glucose; Podocytes; Oxidative stress; OXIDATIVE STRESS; DEATH; APOPTOSIS; BIOLOGY; PATHOGENESIS; MECHANISMS; BECLIN-1; DISEASE; STAGE; LIFE;
D O I
10.1016/j.yexcr.2013.01.018
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Autophagy is a cellular pathway involved in protein and organelle degradation. It is relevant to many types of cellular homeostasis and human diseases. High level of glucose is known to inflict podocyte injury, but little is reported about the relationship between high concentrations of glucose and autophagy in these cells. The present study demonstrates that high glucose promotes autophagy in podocytes. Rapamycin further enhances this effect, but 3-methyadenine inhibits it. The proautophagic effect of high glucose manifested in the form of enhanced podocyte expression of LC3-2 and beclin-1; interestingly, antioxidants such as NAC were found to inhibit high glucose-induced autophagy. High glucose induced the generation of ROS by podocytes in a time-dependent manner. High glucose also enhanced podocyte expression of MnSOD and catalase. These findings indicate that high glucose-induced autophagy is mediated through podocyte ROS generation. (C) 2013 Elsevier Inc. All rights reserved.
引用
收藏
页码:779 / 789
页数:11
相关论文
共 47 条
[1]   MAP-LC3, a promising autophagosomal marker, is processed during the differentiation and recovery of podocytes from PAN nephrosis [J].
Asanuma, K ;
Tanida, I ;
Shirato, I ;
Ueno, T ;
Takahara, H ;
Nishitani, T ;
Kominami, E ;
Tomino, Y .
FASEB JOURNAL, 2003, 17 (06) :1165-+
[2]  
Azad MB, 2009, ANTIOXID REDOX SIGN, V11, P777, DOI 10.1089/ARS.2008.2270
[3]   Autophagy: Dual roles in life and death? [J].
Baehrecke, EH .
NATURE REVIEWS MOLECULAR CELL BIOLOGY, 2005, 6 (06) :505-510
[4]  
Barisoni L, 2009, ARCH PATHOL LAB MED, V133, P201, DOI 10.1043/1543-2165-133.2.201
[5]   Mechanisms Involved in the Genesis of Diabetic Nephropathy [J].
Blazquez-Medela, Ana M. ;
Lopez-Novoa, Jose M. ;
Martinez-Salgado, Carlos .
CURRENT DIABETES REVIEWS, 2010, 6 (02) :68-87
[6]   Is mitochondrial generation of reactive oxygen species a trigger for autophagy? [J].
Chen, Yongqiang ;
Gibson, Spencer B. .
AUTOPHAGY, 2008, 4 (02) :246-248
[7]   Advanced glycation endproducts induce podocyte apoptosis by activation of the FOXO4 transcription factor [J].
Chuang, P. Y. ;
Yu, Q. ;
Fang, W. ;
Uribarri, J. ;
He, J. C. .
KIDNEY INTERNATIONAL, 2007, 72 (08) :965-976
[8]   Autophagy and aging -: The importance of maintaining "clean" cells [J].
Cuervo, Ana Maria ;
Bergamini, Ettore ;
Brunk, Ulf T. ;
Droege, Wulf ;
Ffrench, Martine ;
Terman, Alexei .
AUTOPHAGY, 2005, 1 (03) :131-140
[9]   Oxidative stress as a major culprit in kidney disease in diabetes [J].
Forbes, Josephine M. ;
Coughlan, Melinda T. ;
Cooper, Mark E. .
DIABETES, 2008, 57 (06) :1446-1454
[10]   Life, death and burial: multifaceted impact of autophagy [J].
Galluzzi, Lorenzo ;
Morselli, Eugenia ;
Vicencio, Jose Miguel ;
Kepp, Oliver ;
Joza, Nicholas ;
Tajeddine, Nicolas ;
Kroemer, Guido .
BIOCHEMICAL SOCIETY TRANSACTIONS, 2008, 36 :786-790