2005 Fiscal Year Final Research Report Summary
Redox-regulation by active oxygen species / nitric oxide in cardiovascular system
| Project/Area Number |
15390066
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
General physiology
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| Research Institution | Tokai University |
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Principal Investigator |
NAKAZAWA Hiroe Tokai University, School of Medicine, Professor, 医学部, 教授 (20110885)
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| Co-Investigator(Kenkyū-buntansha) |
ISHIDA Hideyuki Tokai University, School of Medicine, Associate Professor, 医学部, 助教授 (20222424)
FUKUYAMA Naoto Tokai University, School of Medicine, Assistant Professor, 医学部, 講師 (50349338)
TAKEKOSHI Susumu Tokai University, School of Medicine, Associate Professor, 医学部, 助教授 (70216878)
GOTO Shinya Tokai University, School of Medicine, Associate Professor, 医学部, 助教授 (50225653)
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| Project Period (FY) |
2003 – 2005
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| Keywords | Redox / Cardiovascular system / Reactive oxygen species (ROS) / nitric oxide / PAI-1 |
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| Research Abstract |
Purposes
1) 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.
Results
1) 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.
Conclusion
Redox-mediated regulation appears to play an important role on cardiovascular pathogenesis.
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Research Products
(43 results)
