COEXPRESSION OF ICAM-1, VCAM-1, ELAM-1 AND HSP60 IN HUMAN ARTERIAL AND VENOUS ENDOTHELIAL-CELLS IN RESPONSE TO CYTOKINES AND OXIDIZED LOW-DENSITY LIPOPROTEINS

T-cells and monocytes are the first cells infiltrating the arterial in tima during the early stages of atherogenesis, Recently our laboratory has provided evidence that T-cells isolated from atherosclerotic inti ma reacts against heat shock protein 60 (Hsp60). Transmigration of act ivated T-cells into the intima is mediated by adhesion molecules (ICAM -1; VCAM-1; ELAM-1) expressed on activated endothelial cells, Here we studied the potential of cytokines (TNF-alpha, IFN-gamma, IL-l), Esche richia coli lipopolysaccharide (LPS), native and oxidized low-density lipoprotein (LDL; oxLDL) and high temperature to induce adhesion molec ules as well as Hsp60 and Hsp70 expression in human endothelial cells (EC). On Northern blots, a strong signal for ICAM-1, VCAM-1 and ELAM-1 was detected after 4 h, which thereafter declined, but did not reach the basal level of untreated control cells, Heat shock induced the exp ression of Hsp60 and Hsp70 but not of adhesion molecules. EC were cult ivated in serum-free medium, which led to the expression of adhesion m olecule transcripts, Addition of LDL or oxLDL to these ECs did not alt er the expression of these transcripts, The production of adhesion mol ecule proteins was analysed by flow cytometry. In human venous endothe lial cells (HVEC) and human arterial endothelial cells (HAEC) ICAM-1 a nd VCAM-1 production was permanently highly induced, whereas the high level of ELAM-1 production at 4 h disappeared after 24 h, Furthermore, only HAEC, but not HVEC, produced ICAM-1, VCAM-1 and ELAM-1 after str ess by moderately and highly oxLDL, LDL and oxLDL did not induce the p roduction of Hsp60 and Hsp70. The present study demonstrates the co-ex pression of Hsp60 and adhesion molecules in arterial and venous EC in response to cytokine and LPS exposure, and that oxLDL is an efficient inducer of adhesion molecules in arterial EC and not in venous EC. The se features provide the prerequisites for a cellular immune reaction a gainst Hsp60 expressed by stressed EC in the inital stages of atherosc lerosis.