Homocysteine-induced endothelial cell adhesion is related to adenosine lowering and is not mediated by S-adenosylhomocysteine

Cacciapuoti, Giovanna; Manna, Caterina; Napoli, Daniela; Zappia, Vincenzo; Porcelli, Marina

Abstract: 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.

CARDIOVASCULAR diseases; HOMOCYSTEINE; ATHEROSCLEROSIS; CELL adhesion

FEBS Letters, 2007, Vol 581, Issue 24, p4567

0014-5793

Academic Journal

10.1016/j.febslet.2007.08.042