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PGC-1alpha regulates the mitochondrial antioxidant defense system in vascular endothelial cells

Cardiovasc Res. 2005 Jun 1;66(3):562-73. doi: 10.1016/j.cardiores.2005.01.026. Epub 2005 Feb 25.

Abstract

Objective: Mitochondrial production of oxidants contributes to a variety of pathological conditions including the vascular complications of diabetes, neurodegenerative diseases, and cellular senescence. We postulated that a transcriptional coactivator, peroxisome proliferator activated receptor-gamma coactivator 1alpha (PGC-1alpha), a major regulator of oxidative metabolism and mitochondrial biogenesis, could be involved in the transcriptional regulation of the mitochondrial antioxidant defense system in vascular endothelial cells.

Methods and results: We show that PGC-1alpha is present in human, bovine, and mouse endothelial cells and positively modulates the expression of the mitochondrial detoxification system. Endothelial cells that overexpress PGC-1alpha show reduced accumulation of reactive oxygen species (ROS), increased mitochondrial membrane potential, and reduced apoptotic cell death both in basal and oxidative stress conditions. Downregulation of PGC-1alpha levels by siRNA reduces the expression of mitochondrial detoxification proteins.

Conclusions: These results unveil a novel regulatory pathway that links mitochondrial activity and mitochondrial oxidative stress protective systems. In addition, they suggest that PGC-1alpha could play a crucial protective role in vascular complications of diabetes, where the mitochondrial metabolism of glucose has been shown to result in oxidative stress and vascular endothelial cell dysfunction.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis
  • Cattle
  • Cells, Cultured
  • Endothelial Cells / metabolism*
  • Flow Cytometry
  • Gene Expression Regulation
  • Glucose / pharmacology
  • Heat-Shock Proteins / analysis
  • Heat-Shock Proteins / genetics
  • Heat-Shock Proteins / metabolism*
  • Humans
  • Mice
  • Mice, Inbred C57BL
  • Mitochondria / metabolism*
  • Muscle, Smooth, Vascular / metabolism*
  • Oxidative Stress / genetics
  • Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha
  • RNA, Small Interfering / pharmacology
  • Reactive Oxygen Species / metabolism*
  • Transcription Factors / analysis
  • Transcription Factors / genetics
  • Transcription Factors / metabolism*

Substances

  • Heat-Shock Proteins
  • PPARGC1A protein, human
  • Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha
  • RNA, Small Interfering
  • Reactive Oxygen Species
  • Transcription Factors
  • Glucose