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Resistance to pathologic cardiac hypertrophy and reduced expression of CaV1.2 in Trpc3-depleted mice

DC Field Value Language
dc.contributor.author김주영-
dc.contributor.author이민구-
dc.contributor.author이영호-
dc.date.accessioned2017-10-26T07:24:58Z-
dc.date.available2017-10-26T07:24:58Z-
dc.date.issued2016-
dc.identifier.issn0300-8177-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/152000-
dc.description.abstractSustained elevation of intracellular Ca(2+) concentration ([Ca(2+)]i) reprograms cardiovascular cell fate, leading to cellular hypertrophy via Ca(2+)-calmodulin/calcineurin (Cn)/NFAT activation. Accumulating evidence suggests that transient receptor potential canonical (Trpc) channels play important roles in the development of pathologic cardiac hypertrophy. Here, we demonstrated that Trpc3 mediates pathologic cardiac hypertrophy in neurohumoral elevation via direct regulation of CaV1.2 expressions. Elevated PE (phenylephrine) was maintained in mice by continuous infusion using an osmotic pump. Wild-type (WT) mice, but not Trpc3 (-/-) showed a sudden decrease in blood pressure (BP) or death following elevation of BP under conditions of elevated PE. Trpc3 (-/-) mesenteric artery showed decreased PE-stimulated vasoconstriction. Analysis of morphology, function, and pathologic marker expression revealed that PE elevation caused pathologic cardiac hypertrophy in WT mice, which was prevented by deletion of Trpc3. Interestingly, protection by Trpc3 deletion seemed to be a result of reduced cardiac CaV1.2 expressions. Basal and PE induced increased expression of protein and mRNA of CaV1.2 was decreased in Trpc3 (-/-) heart. Accordingly, altered expression of CaV1.2 was observed by knockdown or stimulation of Trpc3 in cardiomyocytes. These findings suggest that Trpc3 is a mediator of pathologic cardiac hypertrophy not only through mediating part of the Ca(2+) influx, but also through control of CaV1.2 expressions.-
dc.description.statementOfResponsibilityrestriction-
dc.languageEnglish-
dc.publisherKluwer Academic-
dc.relation.isPartOfMOLECULAR AND CELLULAR BIOCHEMISTRY-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHAnimals-
dc.subject.MESHCalcium Channels, L-Type/biosynthesis*-
dc.subject.MESHCalcium Channels, L-Type/genetics-
dc.subject.MESHCalcium Signaling*-
dc.subject.MESHCardiomegaly/genetics-
dc.subject.MESHCardiomegaly/metabolism*-
dc.subject.MESHCardiomegaly/pathology-
dc.subject.MESHGene Expression Regulation*-
dc.subject.MESHMesenteric Arteries/metabolism-
dc.subject.MESHMesenteric Arteries/pathology-
dc.subject.MESHMice-
dc.subject.MESHMice, Knockout-
dc.subject.MESHMyocardium/metabolism*-
dc.subject.MESHMyocardium/pathology-
dc.subject.MESHPhenylephrine/metabolism-
dc.subject.MESHTRPC Cation Channels/deficiency*-
dc.subject.MESHVasoconstriction/genetics-
dc.titleResistance to pathologic cardiac hypertrophy and reduced expression of CaV1.2 in Trpc3-depleted mice-
dc.typeArticle-
dc.publisher.locationNetherlands-
dc.contributor.collegeCollege of Medicine-
dc.contributor.departmentDept. of Pharmacology-
dc.contributor.googleauthorJung Woo Han-
dc.contributor.googleauthorYoung Ho Lee-
dc.contributor.googleauthorSu-In Yoen-
dc.contributor.googleauthorJoel Abramowitz-
dc.contributor.googleauthorLutz Birnbaumer-
dc.contributor.googleauthorMin Goo Lee-
dc.contributor.googleauthorJoo Young Kim-
dc.identifier.doi10.1007/s11010-016-2784-0-
dc.contributor.localIdA02781-
dc.contributor.localIdA02968-
dc.contributor.localIdA00942-
dc.relation.journalcodeJ02242-
dc.identifier.eissn1573-4919-
dc.identifier.pmid27522668-
dc.identifier.urlhttps://link.springer.com/article/10.1007%2Fs11010-016-2784-0-
dc.subject.keywordCa2+ influx-
dc.subject.keywordL-type Ca2+ channel-
dc.subject.keywordPathologic cardiac hypertrophy-
dc.subject.keywordTransient receptor potential canonical channels 3-
dc.contributor.alternativeNameKim, Joo Young-
dc.contributor.alternativeNameLee, Min Goo-
dc.contributor.alternativeNameLee, Young Ho-
dc.contributor.affiliatedAuthorLee, Min Goo-
dc.contributor.affiliatedAuthorLee, Young Ho-
dc.contributor.affiliatedAuthorKim, Joo Young-
dc.citation.volume421-
dc.citation.number1~2-
dc.citation.startPage55-
dc.citation.endPage65-
dc.identifier.bibliographicCitationMOLECULAR AND CELLULAR BIOCHEMISTRY, Vol.421(1~2) : 55-65, 2016-
dc.date.modified2017-10-24-
dc.identifier.rimsid46322-
dc.type.rimsART-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Pharmacology (약리학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Physiology (생리학교실) > 1. Journal Papers

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