Redox-regulation by active oxygen species / nitric oxide in cardiovascular system

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Purposes1) To demonstrate active oxygen species/nitric oxide generation from endotherial and smooth muscle cells of coronary artery and cardiac myocytes as initiators of redox-regulation.2) To examine effects of lipoproteins (LDL, HDL, and TG) on PAI-1 secreation endotherial cells from the aspect of redox-regulation.3) To examine redox-regulation in the formation of unstable atheroma using mice atheroma model.Results1) The generation of active oxygen species and nitric oxide from various cells was shown to initial redox-regulation by using electron spin resonance (ESR), chemiluminescence and fluorescence methods.2) In the presence of lipoproteins endotherial cells secreated PAI-1. The amount of PAI-1 secreation was greater in HDL than in LDL additions. These results do not agree with the present knowledge of anti-atherogenic role of HDL. Thus we suggest that the increased PAI-1 in patient with atherosclerosis is not the cause but the consequence.3) Both ApoE^<-/->/iNOS^<-/-> and ApoE^<-/->/iNOS^<+/+> mice fed with atherogenic diet developed comparable size of atheroma. The important difference between the two was atheroma in ApoE^<-/->/iNOS^<+/+> mice was unstable ; less collagen and lipid-rich. Matrix metalloproteinase (MMP) was activated by possibly redox-regulated mechanism though induction of iNOS in ApoE^<-/->/iNOS^<+/+> mice.ConclusionRedox-mediated regulation appears to play an important role on cardiovascular pathogenesis.