Homocysteine alters monocyte-endothelial interaction in vitro.

Objective: To determine whether homocysteine induced endothelial damage through monocyte-endothelial interaction and to characterize both cell types in vitro.

Methods: Radiomethods were performed on monocyte adhesion to/through endothelium and endothelial damage experiments.

Results: Homocysteine-treated endothelial cells increased monocyte adhesion and transmigration.

Leukocytes extravasation in acute homocysteinemic rats.

Homocysteine may promote atherogenesis and thrombogenesis by enhancing leukocyte-endothelium interactions. We explored this hypothesis in an acute hyperhomocysteinemia rat model, which was created by a continuous venous homocysteine infusion (4 ml/h/kg body weight) with 2.5 and 10 mg/ml D,L-homocysteine upto 90 min.

Homocysteine attenuates hemodynamic responses to nitric oxide in vivo.

Homocysteine is a significant but modifiable risk factor for vascular diseases. While several pathological processes may be involved, homocysteine can cause significant endothelial impairment and compromise vascular NO bioactivity. In the present study, we aimed to assess effects of homocysteine on NO-mediated hemodynamic responses in vivo.

Homocysteine induces expressions of adhesive molecules on leukocytes in whole blood.

Objective: To observe whether homocysteine can directly alter the expressions of CD11b, CD18, CD14 and L-selectin on neutrophils, monocytes, and lymphocytes in whole blood from healthy human subjects.

Methods: Leukocyte surface adhesive molecule expressions were analyzed by immunofluorescence flow cytometry.

Results: Homocysteine at the lowest concentration (20 mumol/L) significantly increased surface adhesive molecule expressions of CD11b and CD18 on each cell type and CD14 on monocytes and neutrophils in whole blood.

Interrelations between plasma homocysteine and intracellular S-adenosylhomocysteine.

S-Adenosylhomocysteine, a potent intracellular methylation inhibitor, is suggested as a potential mediator for hyperhomocysteinemia-related vascular changes. We investigated the effect of acute and chronic hyperhomocysteinemia on intracellular S-adenosylhomocysteine and S-adenosylmethionine in rats and humans. Elevated plasma homocysteine in rats infused with homocysteine produced an increase in S-adenosylhomocysteine (P < 0.