Advanced oxidation protein products induce chondrocyte apoptosis via receptor for advanced glycation end products-mediated, redox-dependent intrinsic apoptosis pathway

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• 作者：Qian Wu ; Zhao-Ming Zhong ; Si-Yuan Zhu ; Cong-Rui Liao ; Ying Pan ; Ji-Huan Zeng…
• 关键词：Advanced oxidation protein products ; Rat chondrocyte ; Apoptosis ; Nicotinamide adenine dinucleotide phosphate oxidase ; Reactive oxygen species ; Intrinsic apoptosis pathway
• 刊名：Apoptosis
• 出版年：2016
• 出版时间：January 2016
• 年：2016
• 卷：21
• 期：1
• 页码：36-50
• 全文大小：6,430 KB
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• 作者单位：Qian Wu (1)
  Zhao-Ming Zhong (1)
  Si-Yuan Zhu (1)
  Cong-Rui Liao (1)
  Ying Pan (2)
  Ji-Huan Zeng (3)
  Shuai Zheng (1)
  Ruo-Ting Ding (1)
  Qing-Song Lin (4)
  Qing Ye (1)
  Wen-Bin Ye (1)
  Wei Li (1)
  Jian-Ting Chen (1)
  
  1. Department of Spinal Surgery, Nanfang Hospital, Southern Medical University, 1838 North Guangzhou Avenue, Guangzhou, 510515, China
  2. Department of Oncology, Affiliated Jiujiang Hospital of Nanchang University, Jiujiang, China
  3. Department of Orthopedics, Jiangxi Provincial People’s Hospital, Nanchang, China
  4. Department of Orthopedics, Shekou People’s Hospital, Shenzhen, China
  
• 刊物类别：Medicine
• 刊物主题：Medicine & Public Health
  Oncology
  Cancer Research
  Cell Biology
  Biochemistry
  Virology
  
• 出版者：Springer Netherlands
• ISSN：1573-675X

文摘

Pro-inflammatory cytokine-induced chondrocyte apoptosis is a primary cause of cartilage destruction in the progression of rheumatoid arthritis (RA). Advanced oxidation protein products (AOPPs), a novel pro-inflammatory mediator, have been confirmed to accumulate in patients with RA. However, the effect of AOPPs accumulation on chondrocyte apoptosis and the associated cellular mechanisms remains unclear. The present study demonstrated that the plasma formation of AOPPs was enhanced in RA rats compared with normal. Then, chondrocyte were treated with AOPPs-modified rat serum albumin (AOPPs-RSA) in vitro. Exposure of chondrocyte to AOPPs activated nicotinamide adenine dinucleotide phosphate (NADPH) oxidase and increased expression of NADPH oxidase subunits, which was mediated by receptor for advanced glycation end products (RAGE), but not scavenger receptor CD36. Moreover, AOPPs challenge triggered NADPH oxidase-dependent ROS generation which induced mitochondrial dysfunction and endoplasmic reticulum stress resulted in activation of caspase family that eventually lead to apoptosis. Lastly, blockade of RAGE, instead of CD36, largely attenuated these signals. Our study demonstrated first time that AOPPs induce chondrocyte apoptosis via RAGE-mediated and redox-dependent intrinsic apoptosis pathway in vitro. These data implicates that AOPPs may represent a novel pathogenic factor that contributes to RA progression. Targeting AOPPs-triggered cellular mechanisms might emerge as a promising therapeutic option for patients with RA. Keywords Advanced oxidation protein products Rat chondrocyte Apoptosis Nicotinamide adenine dinucleotide phosphate oxidase Reactive oxygen species Intrinsic apoptosis pathway