2012 Fiscal Year Final Research Report
The development and clinical application of a new oxidative stress marker using glutathionylated protein
| Project/Area Number |
21590902
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Circulatory organs internal medicine
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| Research Institution | Nagasaki University |
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Principal Investigator |
IKEDA Satoshi 長崎大学, 医歯薬学総合研究科, 講師 (10336159)
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| Co-Investigator(Kenkyū-buntansha) |
MAEMURA Koji 長崎大学, 医歯薬学総合研究科, 教授 (90282649)
URATA Yoshishige 長崎大学, 医歯薬学総合研究科, 助教 (30185087)
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| Project Period (FY) |
2009 – 2012
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| Keywords | 臨床心血管病態学 |
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| Research Abstract |
Oxidative stress contributes to the development and progression of atherosclerosis. Reactive oxygen species, major sources of oxidative stress, modifies protein cysteine residues, where a disulfide bond is established between a cysteinyl residue and glutathione, leading to the S-glutathionylation of protein, and this modification can be still reversible. Therefore, we hypothesized a biomarker using S-glutathionylated protein is a good one reflecting an early phase of atherosclerosis. We composed the antibody against S-glutathionylation of apoprotein B100, a component of low-density lipoprotein (LDL) cholesterol. The serum values by immunoblot analysis with this antibody were correlated with negatively charged LDL subfractions, which are induced by oxidative modification, in patients with atherogenetic risks, such as hypertension, diabetes mellitus, and/or dyslipidemia. Immunohistological analysis of carotid endarterectomy sections with the antibody showed S-glutationylated ApoB100 localized at the site close to the vascular lumen, but not the site of foamy cell accumulation. These suggested that serum S-glutationylated ApoB100 may be an oxidative stress marker reflecting the relatively early phase of atherosclerosis.
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Research Products
(6 results)
