Reactive oxygen species mediates homocysteine-induced mitochondrial biogenesis in human endothelial cells: Modulation by antioxidants

Karen Perez-De-Arce, Rocio Foncea, Federico Leighton

Research output: Contribution to journalArticlepeer-review

58 Scopus citations

Abstract

It has been proposed that homocysteine (Hcy)-induces endothelial dysfunction and atherosclerosis by generation of reactive oxygen species (ROS). A previous report has shown that Hcy promotes mitochondrial damage. Considering that oxidative stress can affect mitochondrial biogenesis, we hypothesized that Hcy-induced ROS in endothelial cells may lead to increased mitochondrial biogenesis. We found that Hcy-induced ROS (1.85-fold), leading to a NF-κB activation and increase the formation of 3-nitrotyrosine. Furthermore, expression of the mitochondrial biogenesis factors, nuclear respiratory factor-1 and mitochondrial transcription factor A, was significantly elevated in Hcy-treated cells. These changes were accompanied by increase in mitochondrial mass and higher mRNA and protein expression of the subunit III of cytochrome c oxidase. These effects were significantly prevented by pretreatment with the antioxidants, catechin and trolox. Taken together, our results suggest that ROS is an important mediator of mitochondrial biogenesis induced by Hcy, and that modulation of oxidative stress by antioxidants may protect against the adverse vascular effects of Hcy.

Original languageEnglish (US)
Pages (from-to)1103-1109
Number of pages7
JournalBiochemical and Biophysical Research Communications
Volume338
Issue number2
DOIs
StatePublished - Dec 16 2005

Bibliographical note

Funding Information:
This work was supported by FONDECYT Grant 1020486 (R.F.), and by PUC-PBMEC.

Keywords

  • Antioxidants
  • Gene expression
  • Homocysteine
  • Mitochondrial biogenesis
  • Mitochondrial transcription factor A
  • Nuclear respiratory factor-1
  • Reactive oxygen species

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