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Advanced oxidation protein products induce chondrocyte death through a redox-dependent, poly (ADP-ribose)

Wenbin Ye1, Zhaoming Zhong2, Siyuan Zhu2

  • 1Department of Orthopaedics, The 175th Hospital of PLA, Affiliated Dongnan Hospital of Xiamen University, Zhangzhou, Fujian, China.

Apoptosis : an International Journal on Programmed Cell Death
|November 19, 2016
PubMed

Insights

Advanced Oxidation Protein Products (AOPPs) trigger apoptosis in human chondrocytes via a redox-dependent pathway. Targeting these AOPPs-induced mechanisms may offer new therapies for rheumatoid arthritis (RA).

Area of Science:

  • Biochemistry
  • Cell Biology
  • Rheumatology

Background:

  • Advanced Oxidation Protein Products (AOPPs) are markers of oxidative stress.
  • Oxidative stress plays a role in the pathogenesis of rheumatoid arthritis (RA).
  • The specific effects of AOPPs on human chondrocytes are not fully understood.

Purpose of the Study:

  • To investigate the impact of AOPPs on apoptosis in human chondrocytes.
  • To elucidate the underlying molecular mechanisms of AOPP-induced chondrocyte apoptosis.

Main Methods:

  • Human chondrocytes were treated with AOPPs in vitro.
  • Assays were performed to measure cell death, nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity, reactive oxygen species (ROS) generation, and apoptotic protein expression.
  • AOPPs levels were quantified using a colorimetric method.

Main Results:

  • AOPPs induced significant cell death in human chondrocytes.
  • AOPPs treatment led to increased NADPH oxidase activity and ROS generation.
  • The study observed activation of poly (ADP-ribose) polymerase-1 (PARP-1) and RAGE-mediated pathways.

Conclusions:

  • AOPPs induce apoptosis in human chondrocytes through a redox-dependent pathway.
  • This pathway involves RAGE-mediated, NADPH oxidase-dependent ROS generation and PARP-1 activation.
  • Targeting AOPPs-induced cellular mechanisms presents a potential therapeutic strategy for RA.
Keywords:
Advanced oxidation protein production (AOPPs)ApoptosisChondrocytesOxidative stressPARP-1Rheumatoid arthritis

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