Xuewei Guo1, Nicholas Peter Dudman. 1. Center of Cardiovascular Disease Research, Gansu Province People's Hospital, Lanzhou 730000, China. Xueweiguo@163.net
Abstract
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. Homocysteine-treated monocytes induced endothelial detachment, but this effect was blocked by catalase. These effects were increased with higher concentrations of homocysteine. Monocyte surface glycoprotein antibodies CD11b/CD18 and CD14 inhibited these processes. CONCLUSIONS: Homocysteine alters monocyte-endothelial interaction in vitro, eventually bringing about endothelial damage through release of H(2)O(2). These phenomena are mediated through monocyte surface glycoproteins CD11b/CD18 and CD14. Upregulation of these processes in vivo may contribute to acceleration of atherosclerosis in patients with elevated plasma homocysteine levels.
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. Homocysteine-treated monocytes induced endothelial detachment, but this effect was blocked by catalase. These effects were increased with higher concentrations of homocysteine. Monocyte surface glycoprotein antibodies CD11b/CD18 and CD14 inhibited these processes. CONCLUSIONS:Homocysteine alters monocyte-endothelial interaction in vitro, eventually bringing about endothelial damage through release of H(2)O(2). These phenomena are mediated through monocyte surface glycoproteins CD11b/CD18 and CD14. Upregulation of these processes in vivo may contribute to acceleration of atherosclerosis in patients with elevated plasma homocysteine levels.