ABSTRACT
Objective The processes responsible for the uptake of very low density lipoprotein(VLDL) by monocyte macrophage cells were investigated. Methods The effects of VLDL concentration, apoE ligand activity and scavenger receptor A (SRA) on the binding of 125 I VLDL to monocyte macrophages were analysed. The influence of VLDL on SRA mRNA and protein expression and VLDL receptor gene translation was probed. Results (1) The differentiated monocyte macrophages induced 125 I VLDL uptake by dose dependent pathway( r =0 71, P
ABSTRACT
AIM: To determine the role of LOX-1/PPAR pathway in regulating expression of adhesion molecules elicited by oxidizing low density lipoprotein(Ox-LDL) through Lectin-like oxidized low-density lipoprotein receptor-1(LOX-1) in human umbilical vein endothelial cells(HUVECs).METHODS: HUVECs were incubated with Ox-LDL,poly(I),carrageenan or 15-deoxy-△12,14-prostaglanding J2(15d-PGJ2).PPAR mRNA and protein were examined by real time RT-PCR and Western blotting.ICAM-1 and E-selectin were detected by RT-PCR and Western blotting respectively.RESULTS: Ox-LDL increased PPAR expression in HUVECs,which was inhibited by pretreatment of HUVECs with LOX-1 blockers.Preincubation of HUVECs with 15d-PGJ2 attenuated the expression of intercellular adhesion molecule-1(ICAM-1) and E-selectin in response to Ox-LDL.Upregulation of ICAM-1 and E-selectin mediated by Ox-LDL were suppressed more significantly by the combination of 15d-PGJ2 and polyinosonic acid as compared to either 15d-PGJ2 or polyinosonic acid alone.CONCLUSION: The results indicate that Ox-LDL exerts a biphasic effects on inflammatory response.It evokes harmful effects by inflammatory injury on one side and protective effects by triggering the LOX-1/ PPAR signaling pathway on the other hand.