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Comparison of contractile mechanisms of sphingosylphosphorylcholine and sphingosine-1-phosphate in rabbit coronary artery

DC FieldValueLanguage
dc.contributor.author안덕선-
dc.contributor.author이영호-
dc.contributor.author최수경-
dc.date.accessioned2015-04-24T16:33:43Z-
dc.date.available2015-04-24T16:33:43Z-
dc.date.issued2009-
dc.identifier.issn0008-6363-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/103745-
dc.description.abstractAIMS: Although stimulation with sphingosylphosphorylcholine (SPC) or sphingosine-1-phosphate (S1P) generally leads to similar vascular responses, the contractile patterns and their underlying signalling mechanisms are often distinct. We investigated the different reliance upon Ca2+-dependent and Ca2+-sensitizing mechanisms of constriction in response to SPC or S1P in coronary arteries. METHODS AND RESULTS: Contractile responses, changes in [Ca2+]i, and phosphorylation of myosin light chain phosphatase-targeting subunit (MYPT1) were measured. SPC induced a concentration-dependent sustained contraction. S1P evoked a rapid rise in force (initial transient), which was followed by a secondary sustained force. In the absence of extracellular Ca2+, the concentration dependency of constriction to SPC was shifted to the right, but with no change in maximum force, whereas S1P-induced contraction was significantly blunted. Cyclopiazonic acid (CPA) significantly decreased the initial transient force induced by S1P. In isolated single cells, S1P markedly increased [Ca2+]i, whereas only a modest elevation was noted with SPC. The S1P-induced elevation of [Ca2+]i was abolished by pre-treatment with CPA and was significantly reduced in the absence of extracellular Ca2+. In beta-escin-permeabilized strips, SPC augmented pCa 6.3-induced force; this was significantly inhibited by fasudil hydrochloride. S1P induced little or no augmentation of pCa 6.3-induced force. In intact arteries, SPC-induced contraction was completely inhibited by fasudil hydrochloride. Fasudil hydrochloride had no effect on the initial transient force induced by S1P but significantly inhibited the secondary sustained force. SPC induced a several-fold increase in Thr696 and Thr853 phosphorylation of MYPT1, but S1P did not affect phosphorylation of MYPT1. CONCLUSION: Our results suggest that constriction of coronary arteries in response to the bioactive lipid S1P or SPC occurs by distinct signalling pathways. Activation of the RhoA/RhoA-associated kinase pathway and subsequent phosphorylation of MYPT1 play a key role in SPC-induced coronary contraction, whereas elevation of [Ca2+]i is crucial for S1P-induced coronary constriction.-
dc.description.statementOfResponsibilityopen-
dc.format.extent324~332-
dc.relation.isPartOfCARDIOVASCULAR RESEARCH-
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/metabolism-
dc.subject.MESHCoronary Vessels/cytology-
dc.subject.MESHCoronary Vessels/drug effects-
dc.subject.MESHCoronary Vessels/metabolism*-
dc.subject.MESHDose-Response Relationship, Drug-
dc.subject.MESHEnzyme Inhibitors/pharmacology-
dc.subject.MESHIndoles/pharmacology-
dc.subject.MESHLysophospholipids/metabolism-
dc.subject.MESHLysophospholipids/pharmacology*-
dc.subject.MESHMuscle Contraction/drug effects*-
dc.subject.MESHMuscle, Smooth, Vascular/cytology-
dc.subject.MESHMuscle, Smooth, Vascular/drug effects-
dc.subject.MESHMuscle, Smooth, Vascular/metabolism*-
dc.subject.MESHMyosin-Light-Chain Phosphatase/metabolism-
dc.subject.MESHPhosphorylation-
dc.subject.MESHPhosphorylcholine/analogs & derivatives*-
dc.subject.MESHPhosphorylcholine/metabolism-
dc.subject.MESHPhosphorylcholine/pharmacology-
dc.subject.MESHRabbits-
dc.subject.MESHSarcoplasmic Reticulum/metabolism-
dc.subject.MESHSignal Transduction/physiology*-
dc.subject.MESHSphingosine/analogs & derivatives*-
dc.subject.MESHSphingosine/metabolism-
dc.subject.MESHSphingosine/pharmacology-
dc.subject.MESHrho-Associated Kinases/metabolism-
dc.titleComparison of contractile mechanisms of sphingosylphosphorylcholine and sphingosine-1-phosphate in rabbit coronary artery-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Physiology (생리학)-
dc.contributor.googleauthorSoo-Kyoung Choi-
dc.contributor.googleauthorDuck-Sun Ahn-
dc.contributor.googleauthorYoung-Ho Lee-
dc.identifier.doi10.1093/cvr/cvp054-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA02223-
dc.contributor.localIdA02968-
dc.contributor.localIdA04091-
dc.relation.journalcodeJ00464-
dc.identifier.eissn1755-3245-
dc.identifier.pmid19218288-
dc.subject.keywordSphingosylphosphorylcholine-
dc.subject.keywordSphingosine-1-phosphate-
dc.subject.keyword[Ca2+]I-
dc.subject.keywordRhoA/RhoA-associated kinase-
dc.subject.keywordRabbit coronary artery-
dc.contributor.alternativeNameAhn, Duk Sun-
dc.contributor.alternativeNameLee, Young Ho-
dc.contributor.alternativeNameChoi, Soo Kyoung-
dc.contributor.affiliatedAuthorAhn, Duk Sun-
dc.contributor.affiliatedAuthorLee, Young Ho-
dc.contributor.affiliatedAuthorChoi, Soo Kyoung-
dc.citation.volume82-
dc.citation.number2-
dc.citation.startPage324-
dc.citation.endPage332-
dc.identifier.bibliographicCitationCARDIOVASCULAR RESEARCH, Vol.82(2) : 324-332, 2009-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Physiology (생리학교실) > 1. Journal Papers

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