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Homocysteine‐induced endothelial cell adhesion is related to adenosine lowering and is not mediated by S ‐adenosylhomocysteine
Author(s) -
Cacciapuoti Giovanna,
Manna Caterina,
Napoli Daniela,
Zappia Vincenzo,
Porcelli Marina
Publication year - 2007
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2007.08.042
Subject(s) - adenosine , homocysteine , hyperhomocysteinemia , intracellular , chemistry , cell adhesion , endothelial stem cell , biochemistry , adhesion , cell , endothelium , microbiology and biotechnology , endocrinology , biology , in vitro , organic chemistry
Hyperhomocysteinemia is a cardiovascular risk factor and may contribute to the pathogenesis of atherosclerosis by altering endothelial functions. The mechanism of homocysteine‐induced cell adhesion has been here investigated using EA.hy 926 cells. Homocysteine induces a stereospecific, time‐ and dose‐dependent cell adhesion which is prevented by adenosine. The dramatic increase of S ‐adenosylhomocysteine induced by adenosine‐2′,3′‐dialdehyde does not cause cell adhesion, indicating that no apparent relationship exists between this process and intracellular S ‐adenosylhomocysteine content. Homocysteine‐induced cell adhesion is abolished by pre‐treatment with adenosine‐2′,3′‐dialdehyde, demonstrating that the adenosine depletion caused by reversal of S ‐adenosylhomocysteine hydrolase reaction is responsible for homocysteine‐induced cell damage.