A point mutant of apolipoprotein A-I, V156K, exhibited potent anti-oxidant and anti-atherosclerotic activity in hypercholesterolemic C57BL/6 mice = 항산화 및 항동맥경화 활성 보유 아포지단백질 변이체 V156K

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dc.contributor.authorK H Cho-
dc.contributor.authorS H Park-
dc.contributor.authorJong Min Han-
dc.contributor.authorHyoung-Chin Kim-
dc.contributor.authorI Choi-
dc.contributor.authorJ R Kim-
dc.date.accessioned2017-04-19T09:07:00Z-
dc.date.available2017-04-19T09:07:00Z-
dc.date.issued2007-
dc.identifier.issnI000-0028-
dc.identifier.uri10.1038/emm.2007.18ko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/7881-
dc.description.abstractIn our previous study, two point mutants of apolipoprotein A-I, designated V156K and A158E, revealed peculiar characteristics in their lipid-free and lipid-bound states. In order to determine the putative therapeutic potential of these mutants, several in vitro and in vivo evaluations were conducted. In the lipid-free state, V156K showed more profound antioxidant activity against LDL oxidation than did the wildtype (WT) or A158E variants in an in vitro assay. In the lipid-bound state, V156K-rHDL showed an enhanced cholesterol delivery activity to HepG2 cells in a time-dependent manner, as compared to WT-rHDL, A158E-rHDL, and R173C-rHDL. We assessed the physiological activities of the mutants in circulation, using hypercholesterolemic mice (C57BL6/J). Palmitoyloleoyl phosphatidylcholine (POPC)-rHDL preparations containing each of the apoA-I variants were injected into the mice at a dosage of 30 mg of apoA-I/kg of body weight. Forty eight hours after injection, the sera of the V156K-rHDL injected group showed the most potent antioxidant abilities in the ferric acid removal assay. The V156K-rHDL- or R173C-rHDL-injected mice showed no atherosclerotic lesions and manifested striking increases in their serum apo-E levels, as compared to the mice injected with WT-rHDL or A158E-rHDL. In conclusion, V156K-rHDL exhibited the most pronounced antioxidant activity and anti-atherosclerotic activity, both in vitro and in vivo. These results support the notion that HDL-therapy may prove beneficial due to its capacity to induce accelerated cholesterol excretion, as well as its enhanced antioxidant and anti-inflammatory effects and lesion regression effect.-
dc.publisherSpringer-Nature Pub Group-
dc.titleA point mutant of apolipoprotein A-I, V156K, exhibited potent anti-oxidant and anti-atherosclerotic activity in hypercholesterolemic C57BL/6 mice = 항산화 및 항동맥경화 활성 보유 아포지단백질 변이체 V156K-
dc.title.alternativeA point mutant of apolipoprotein A-I, V156K, exhibited potent anti-oxidant and anti-atherosclerotic activity in hypercholesterolemic C57BL/6 mice-
dc.typeArticle-
dc.citation.titleExperimental and Molecular Medicine-
dc.citation.number2-
dc.citation.endPage169-
dc.citation.startPage160-
dc.citation.volume39-
dc.contributor.affiliatedAuthorJong Min Han-
dc.contributor.affiliatedAuthorHyoung-Chin Kim-
dc.contributor.alternativeName조경현-
dc.contributor.alternativeName박선현-
dc.contributor.alternativeName한종민-
dc.contributor.alternativeName김형진-
dc.contributor.alternativeName최인호-
dc.contributor.alternativeName김재령-
dc.identifier.bibliographicCitationExperimental and Molecular Medicine, vol. 39, no. 2, pp. 160-169-
dc.identifier.doi10.1038/emm.2007.18-
dc.subject.keywordAntioxidants-
dc.subject.keywordApolipoprotein A-I-
dc.subject.keywordAtherosclerosis-
dc.subject.keywordHDL-
dc.subject.keywordLipoproteins-
dc.subject.keywordMutant proteins-
dc.subject.localAntioxidants-
dc.subject.localantioxidant-
dc.subject.localAnti-oxidant-
dc.subject.localantioxidants-
dc.subject.localANTIOXIDANT-
dc.subject.localanti-oxidants-
dc.subject.localAntioxidant-
dc.subject.localApolipoprotein A-I-
dc.subject.localapolipoprotein A-I-
dc.subject.localatherosclerosis-
dc.subject.localAtherosclerosis-
dc.subject.localatheroclerosis-
dc.subject.localHDL-
dc.subject.localLipoproteins-
dc.subject.locallipoprotein-
dc.subject.localLipoprotein-
dc.subject.locallipoproteins-
dc.subject.localMutant proteins-
dc.description.journalClassY-
Appears in Collections:
Ochang Branch Institute > Division of National Bio-Infrastructure > Laboratory Animal Resource & Research Center > 1. Journal Articles
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