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Related Experiment Videos

Mitochondrial glutathione modulates TNF-alpha-induced endothelial cell dysfunction.

K H Chen1, L M Reece, J F Leary

  • 1Sealy Center for Molecular Cardiology, Department of Internal Medicine, The University of Texas Medical Branch, Galveston 77555-0609, USA. khchen@utmb.edu

Free Radical Biology & Medicine
|August 12, 1999
PubMed
Summary

Mitochondrial glutathione (GSH) depletion enhances tumor necrosis factor-alpha (TNF-alpha)-induced adhesion molecule expression and leukocyte adhesion in endothelial cells by increasing reactive oxygen species (ROS). Cytoplasmic GSH depletion had minimal effects.

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Area of Science:

  • Endothelial cell biology
  • Molecular immunology
  • Biochemistry

Background:

  • Tumor necrosis factor-alpha (TNF-alpha) plays a role in inflammation.
  • Glutathione (GSH) is a key intracellular antioxidant.
  • Endothelial cell activation involves adhesion molecule expression.

Purpose of the Study:

  • To investigate the role of glutathione (GSH) depletion in TNF-alpha-induced endothelial cell activation.
  • To determine the specific contribution of cytoplasmic versus mitochondrial GSH to this process.

Main Methods:

  • Human umbilical vein endothelial cells (HUVECs) were treated with L-buthionine-[S,R]-sulphoximine (BSO) to deplete GSH.
  • TNF-alpha was used to induce adhesion molecule expression (E-selectin, VCAM-1, ICAM-1).
  • Mononuclear leukocyte adhesion and reactive oxygen species (ROS) generation were measured.

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Main Results:

  • Depletion of mitochondrial GSH, but not cytoplasmic GSH, markedly enhanced TNF-alpha-induced E-selectin and VCAM-1 expression.
  • TNF-alpha-induced ICAM-1 expression was unaffected by GSH depletion.
  • Mitochondrial GSH depletion led to increased ROS generation and enhanced mononuclear leukocyte adhesion.

Conclusions:

  • Mitochondrial GSH plays a critical role in regulating TNF-alpha-induced adhesion molecule expression and leukocyte adhesion in HUVECs.
  • Depletion of mitochondrial GSH increases ROS generation, contributing to endothelial cell activation.
  • Targeting mitochondrial GSH may offer therapeutic potential in inflammatory conditions.