Homocysteine accelerates endothelial cell senescence

Dong Xu, Richard Neville, Toren Finkel*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

177 Scopus citations

Abstract

In this study we demonstrate that exposure of cultured endothelial cells to homocysteine significantly accelerates the rate of endothelial senescence. Examination of telomere length demonstrates that homocysteine increases the amount of telomere length lost per population doubling. The effects of homocysteine on both senescence and telomere length are inhibited by treatment with the peroxide scavenger catalase. Chronic exposure of endothelial cells to homocysteine also increases the expression of two surface molecules linked to vascular disease, intracellular adhesion molecule-1 (ICAM-1) and plasminogen activator inhibitor-1 (PAI-1). Interestingly, the level of expression of both ICAM-1 and PAI-1 correlates with the degree of endothelial senescence. Taken together, these results suggest that homocysteine accelerates the rate of cellular senescence through a redox-dependent pathway. In addition, it suggests that chronic oxidative stress in the vessel wall may hasten the rate of senescence and that the senescent endothelial cell may in turn be pro-atherogenic. (C) 2000 Federation of European Biochemical Societies.

Original languageEnglish (US)
Pages (from-to)20-24
Number of pages5
JournalFEBS Letters
Volume470
Issue number1
DOIs
StatePublished - Mar 17 2000

Keywords

  • Aging
  • Atherosclerosis
  • Intracellular adhesion molecule-1
  • Redox
  • Telomere

ASJC Scopus subject areas

  • Biophysics
  • Structural Biology
  • Biochemistry
  • Molecular Biology
  • Genetics
  • Cell Biology

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