Rat Aortic Endothelial Cells Of Nf-¦Êb Activation And Pdgf-b Expression

Atherosclerosis is a complicated disease involving multiple risk factors. Among which, hyperlipidemia and hypertension are considered as two important and independent risk factors.It's well known that oxidized density lipoprotein (oxLDL) and/or minimally modified low density lipoprotein (mmLDL) play a very important role during atherogenesis, mostly by accelerating the oxidation of serum lipid in hyperlipidemic patients. OxLDL is known able to promote cytokines expression in monocytes, for instance, TNF-α, and also enables to increase the production of intracellular reactive oxygen species in endothelial cells, thus activates nuclear factor-kappa B (NF-kB) in vitro. It was reported that mm-LDL could activate NF-kB, inducing adhesion of monocytes to endothelial cells. Data of our previous experiment indicated that mm-LDL activated NF-kB in endothelial cells via NIK-IKK pathway and promoted the expression of PDGF-b in vitro.In case of hypertension, it's recognized that rennin-angiotensin system has significant effect on the development of hypertension. Angiotensin II (Ang II) is the major effector of this system and most of the reactions induced by Ang II are through the type 1 receptors (ATI). Recently, losartan, a drug highly selective in inhibiting the activity of AT1 receptor, was used clinically as the antagonist. In addition, Muller DN et al. reported in 2000 that inhibition of NF-kB activation can ameliorate the inflammatory damage in rats. It was also reported that Ang II could induce the expression of PDGF. The previous result in this laboratory also demonstrated that Ang II was effective in activating NF-kB and inducing PDGF-b transcription in endothelial cell line ECV304.NF-kB is a transcription factor family including p65 (RelA), p50 (NF-kB-1), c-Rel, RelB, p52 (NF-kB-2), v-Rel, c-Rel, Drosal and Dif in drosophila. The NH₂-end of this transcription factor family has a conserved 300 amino acids named Rel homogenous...