232 430

Cited 20 times in

Transient receptor potential canonical type 3 channels control the vascular contractility of mouse mesenteric arteries

DC Field Value Language
dc.contributor.author연수인-
dc.contributor.author이영호-
dc.contributor.author김주영-
dc.date.accessioned2015-01-06T17:26:59Z-
dc.date.available2015-01-06T17:26:59Z-
dc.date.issued2014-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/100000-
dc.description.abstractTransient receptor potential canonical type 3 (TRPC3) channels are non-selective cation channels and regulate intracellular Ca2+ concentration. We examined the role of TRPC3 channels in agonist-, membrane depolarization (high K+)-, and mechanical (pressure)-induced vasoconstriction and vasorelaxation in mouse mesenteric arteries. Vasoconstriction and vasorelaxation of endothelial cells intact mesenteric arteries were measured in TRPC3 wild-type (WT) and knockout (KO) mice. Calcium concentration ([Ca2+]) was measured in isolated arteries from TRPC3 WT and KO mice as well as in the mouse endothelial cell line bEnd.3. Nitric oxide (NO) production and nitrate/nitrite concentrations were also measured in TRPC3 WT and KO mice. Phenylephrine-induced vasoconstriction was reduced in TRPC3 KO mice when compared to that of WT mice, but neither high K+- nor pressure-induced vasoconstriction was altered in TRPC3 KO mice. Acetylcholine-induced vasorelaxation was inhibited in TRPC3 KO mice and by the selective TRPC3 blocker pyrazole-3. Acetylcholine blocked the phenylephrine-induced increase in Ca2+ ratio and then relaxation in TRPC3 WT mice but had little effect on those outcomes in KO mice. Acetylcholine evoked a Ca2+ increase in endothelial cells, which was inhibited by pyrazole-3. Acetylcholine induced increased NO release in TRPC3 WT mice, but not in KO mice. Acetylcholine also increased the nitrate/nitrite concentration in TRPC3 WT mice, but not in KO mice. The present study directly demonstrated that the TRPC3 channel is involved in agonist-induced vasoconstriction and plays important role in NO-mediated vasorelaxation of intact mesenteric arteries.-
dc.description.statementOfResponsibilityopen-
dc.format.extente110413-
dc.relation.isPartOfPLOS ONE-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHAcetylcholine/pharmacology-
dc.subject.MESHAnimals-
dc.subject.MESHCalcium/metabolism-
dc.subject.MESHEndothelial Cells/drug effects-
dc.subject.MESHEndothelial Cells/metabolism-
dc.subject.MESHMesenteric Arteries/metabolism*-
dc.subject.MESHMice-
dc.subject.MESHMice, Knockout-
dc.subject.MESHModels, Animal-
dc.subject.MESHMuscle, Smooth, Vascular/drug effects-
dc.subject.MESHMuscle, Smooth, Vascular/metabolism-
dc.subject.MESHNitric Oxide/biosynthesis-
dc.subject.MESHTRPC Cation Channels/genetics*-
dc.subject.MESHTRPC Cation Channels/metabolism-
dc.subject.MESHVasoconstriction/drug effects-
dc.subject.MESHVasoconstriction/genetics*-
dc.subject.MESHVasodilation/drug effects-
dc.subject.MESHVasodilation/genetics-
dc.titleTransient receptor potential canonical type 3 channels control the vascular contractility of mouse mesenteric arteries-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Physiology (생리학)-
dc.contributor.googleauthorSoo-In Yeon-
dc.contributor.googleauthorJoo Young Kim-
dc.contributor.googleauthorDong-Soo Yeon-
dc.contributor.googleauthorJoel Abramowitz-
dc.contributor.googleauthorLutz Birnbaumer-
dc.contributor.googleauthorShmuel Muallem-
dc.contributor.googleauthorYoung-Ho Lee-
dc.identifier.doi10.1371/journal.pone.0110413-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA00942-
dc.contributor.localIdA02350-
dc.contributor.localIdA02968-
dc.relation.journalcodeJ02540-
dc.identifier.eissn1932-6203-
dc.identifier.pmid25310225-
dc.contributor.alternativeNameYeon, Soo In-
dc.contributor.alternativeNameLee, Young Ho-
dc.contributor.alternativeNameKim, Joo Young-
dc.contributor.affiliatedAuthorKim, Joo Young-
dc.contributor.affiliatedAuthorYeon, Soo In-
dc.contributor.affiliatedAuthorLee, Young Ho-
dc.citation.volume9-
dc.citation.number10-
dc.citation.startPagee110413-
dc.identifier.bibliographicCitationPLOS ONE, Vol.9(10) : e110413, 2014-
dc.identifier.rimsid54400-
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

qrcode

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.