Homocysteine accelerates endothelial cell senescence

FEBS Letters

Finkel, Toren²  Neville, Richard¹  Xu, Dong² 

[1] Department of Surgery, Georgetown School of Medicine, Washington, DC, USA;Laboratory of Molecular Biology, NHLBI, NIH, Bldg 10/7B-15, 10 Center Drive, Bethesda, MD 20892-1650, USA

关键词: Atherosclerosis;    Intracellular adhesion molecule-1;    Redox;    Telomere;    Aging;   

DOI  :  10.1016/S0014-5793(00)01278-3

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

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.

【 授权许可】

Unknown