Abstract-Postnatal

(22% ؎ 2% versus 13% ؎ 3%, P < .05 and KDR (49% ؎ 12% versus 19% ؎ 7%, P < .05). Fluorescence and confocal laser microscopy demonstrated the uptake of apoptotic bodies by the EPCs. Apoptotic bodies-depleted medium had no effect, whereas the incubation with suspension of apoptotic bodies induced effects similar to those of ABRM. Our results suggest that apoptotic bodies from ECs are taken up by EPCs, increasing their number and differentiation state. Such a mechanism may facilitate the repair of injured endothelium and may represent a new signaling pathway between progenitor and damaged somatic cells.

Cell adhesion to endothelial cells stimulated by tumor necrosis factor-a (TNF) is due to induction of surface receptors, such as vascular cell adhesion molecule-1 (VCAM-1). The antiaxidant pyrrolidine dithiocarbamate (PDTC) specifically inhibits activation of nuclear factor-KB (NF-KB). Since *B motifs are present in VCAM-1 and intercellular adhesion molecule-1 (ICAM-1) promoters, we used PDTC to study the regulatory mechanisms of VCAM-1 and ICAM-1 induction and subsequent monocyte adhesion in TNF-treated human umbilical vein endothelial cells (HUVECs). PDTC or JV-acetylcysteine dose dependently reduced TNF-induced VCAM-1 but not ICAM-1 surface protein (also in human umbilical arterial endothelial cells) and mRNA expression (by 70% at 100 junol/L PDTC) in HUVECs as assessed by flow cytometry and porymerase chain reaction. Gel-shift analysis in HUVECs demonstrated that PDTC prevented NF-KB mobilization by TNF, suggesting that only VCAM-1 induction was controlled by NF-KB. Since HUVECs released superoxide anions in response to TNF, and H 2 O 2

The reduction of CD11b expression and inhibition of CD11b-dependent monocyte adhesion to endothelium may crucially contribute to the clinical benefit of HMG-CoA reductase inhibitors in CHD, independent of cholesterol-lowering effects.

Our data suggest that aspirin inhibits NF-kappa B mobilization, induction of VCAM-1 and E-selectin, and subsequent monocyte adhesion in endothelial cells stimulated by TNF, thereby providing an additional mechanism for therapeutic effects of aspirin.