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Mitochondrial ATP synthase is a target for TNBS-induced protein carbonylation in XS-106 dendritic cells

Jeong Hwan Je1, Tae Hyung Lee, Dong Hyun Kim

  • 1Department of Dermatology and Cutaneous Biology Research Institute, Brain Korea 21 Project for Medical Science, Yonsei University College of Medicine, Seoul, Korea.

Proteomics
|June 20, 2008
PubMed

Insights

Reactive oxygen species (ROS) cause protein carbonylation in dendritic cells (DCs) during contact hypersensitivity (CHS). TNBS allergen exposure led to mitochondrial ATP synthase carbonylation, a key finding in CHS.

Area of Science:

  • Immunology
  • Oxidative Stress Biology

Background:

  • Reactive oxygen species (ROS) are integral to dendritic cell (DC) function during antigen presentation in contact hypersensitivity (CHS).
  • Protein carbonylation, a marker of oxidative stress, occurs due to ROS-induced nonenzymatic protein modifications.

Purpose of the Study:

  • To identify proteins carbonylated in DCs following exposure to 2,4,6-trinitrobenzene sulfonic acid (TNBS), a known contact allergen.
  • To investigate the role of ROS in TNBS-induced protein carbonylation within DCs.

Main Methods:

  • Utilized the mouse DC line XS-106 and human monocyte-derived DCs (Mo-DCs).
  • Assessed ROS production, myeloperoxidase (MPO) levels, and IL-12 production.
  • Employed MALDI-TOF analysis and 2-D Western blotting to detect protein carbonylation.
  • Investigated the effect of glutathione (GSH) on ROS and carbonylation.

Main Results:

  • TNBS exposure induced ROS production and increased IL-12 levels in DCs.
  • TNBS significantly induced carbonylation of mitochondrial adenosine triphosphate (ATP) synthase in XS-106 DCs.
  • ROS production and protein carbonylation were confirmed in human Mo-DCs.
  • Glutathione (GSH) administration reduced ROS and protein carbonylation in Mo-DCs.

Conclusions:

  • TNBS-induced ROS leads to significant protein carbonylation in DCs, notably affecting mitochondrial ATP synthase.
  • Carbonylation of ATP synthase in DCs may play a role in the pathogenesis of CHS.
  • These findings highlight a specific molecular mechanism linking oxidative stress to allergic contact dermatitis.

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