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Homocysteine accelerates endothelial cell senescence.
1Laboratory of Molecular Biology, NHLBI, NIH, Bldg 10/7B-15, 10 Center Drive, Bethesda, MD 20892-1650, USA.
FEBS Letters
|March 21, 2000
Summary
Homocysteine accelerates endothelial cell senescence and telomere shortening, a process linked to oxidative stress. This cellular aging may contribute to the development of vascular diseases like atherosclerosis.
Area of Science:
- Cellular Biology
- Cardiovascular Research
- Oxidative Stress Studies
Background:
- Endothelial cells form the inner lining of blood vessels.
- Cellular senescence is a state of irreversible growth arrest.
- Elevated homocysteine levels are associated with cardiovascular disease.
Purpose of the Study:
- To investigate the effect of homocysteine on endothelial cell senescence.
- To determine the role of oxidative stress in homocysteine-induced senescence.
- To examine the relationship between endothelial senescence and markers of vascular disease.
Main Methods:
- Cultured human endothelial cells were exposed to homocysteine.
- Telomere length was measured to assess cellular aging.
- Expression of intercellular adhesion molecule-1 (ICAM-1) and plasminogen activator inhibitor-1 (PAI-1) was analyzed.
- Catalase, a peroxide scavenger, was used to investigate the role of oxidative stress.
Main Results:
- Homocysteine exposure significantly accelerated endothelial cell senescence and telomere shortening.
- The effects of homocysteine were mitigated by catalase treatment, indicating a redox-dependent mechanism.
- Chronic homocysteine exposure increased the expression of ICAM-1 and PAI-1.
- ICAM-1 and PAI-1 expression levels correlated with the degree of endothelial senescence.
Conclusions:
- Homocysteine accelerates endothelial senescence via a redox-dependent pathway.
- Oxidative stress in the vessel wall may promote cellular senescence.
- Senescent endothelial cells could play a pro-atherogenic role in vascular disease development.