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Homocysteine-induced decrease in endothelin-1 production is initiated at the extracellular level and involves

S Drunat1, N Moatti, J L Paul

  • 1Laboratoire de Biochimie Appliquée et IFR ISIT, Faculté de Pharmacie, Université Paris XI, Châtenay-Malabry, France.

European Journal of Biochemistry
|October 19, 2001
PubMed
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Extracellular homocysteine (Hcy) accumulation, not intracellular, impairs endothelial cell function. This extracellular Hcy triggers reduced endothelin-1 (ET-1) production via oxidative stress, contributing to cardiovascular risk.

Area of Science:

  • Cardiovascular Science
  • Endothelial Cell Biology
  • Biochemistry

Background:

  • Hyperhomocysteinemia is linked to cardiovascular disease, partly due to homocysteine (Hcy)-induced endothelial dysfunction.
  • The precise location (intracellular vs. extracellular) of Hcy interaction initiating endothelial dysfunction remains unclear.

Purpose of the Study:

  • To investigate the distinct effects of intracellular and extracellular homocysteine accumulation on endothelin-1 (ET-1) synthesis in human endothelial cells.
  • To elucidate the role of extracellular Hcy in endothelial cell dysfunction.

Main Methods:

  • Cultured human endothelial cells were incubated with methionine or homocysteine (Hcy) at varying concentrations.
  • The impact of amino acid transport inhibitors and extracellular free-radical scavengers on Hcy effects was assessed.

Related Experiment Videos

  • Cellular Hcy content and endothelin-1 (ET-1) production were quantified.

    • Main Results:

    • Extracellular Hcy accumulation significantly reduced ET-1 production.
    • Increased intracellular Hcy content did not correlate with reduced ET-1 production.
    • Extracellular free-radical inhibitors attenuated the Hcy-induced decrease in ET-1, suggesting oxidative stress involvement.

    Conclusions:

    • Extracellular Hcy accumulation, rather than intracellular, is the primary trigger for reduced ET-1 production in endothelial cells.
    • Oxidative products generated by extracellular Hcy contribute to endothelial dysfunction.
    • Findings clarify the mechanism linking hyperhomocysteinemia to endothelial cell dysfunction and cardiovascular risk.