Cited 32 times in
Comparison of contractile mechanisms of sphingosylphosphorylcholine and sphingosine-1-phosphate in rabbit coronary artery
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 안덕선 | - |
dc.contributor.author | 이영호 | - |
dc.contributor.author | 최수경 | - |
dc.date.accessioned | 2015-04-24T16:33:43Z | - |
dc.date.available | 2015-04-24T16:33:43Z | - |
dc.date.issued | 2009 | - |
dc.identifier.issn | 0008-6363 | - |
dc.identifier.uri | https://ir.ymlib.yonsei.ac.kr/handle/22282913/103745 | - |
dc.description.abstract | AIMS: 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.statementOfResponsibility | open | - |
dc.format.extent | 324~332 | - |
dc.relation.isPartOf | CARDIOVASCULAR RESEARCH | - |
dc.rights | CC BY-NC-ND 2.0 KR | - |
dc.rights.uri | https://creativecommons.org/licenses/by-nc-nd/2.0/kr/ | - |
dc.subject.MESH | Animals | - |
dc.subject.MESH | Calcium/metabolism | - |
dc.subject.MESH | Coronary Vessels/cytology | - |
dc.subject.MESH | Coronary Vessels/drug effects | - |
dc.subject.MESH | Coronary Vessels/metabolism* | - |
dc.subject.MESH | Dose-Response Relationship, Drug | - |
dc.subject.MESH | Enzyme Inhibitors/pharmacology | - |
dc.subject.MESH | Indoles/pharmacology | - |
dc.subject.MESH | Lysophospholipids/metabolism | - |
dc.subject.MESH | Lysophospholipids/pharmacology* | - |
dc.subject.MESH | Muscle Contraction/drug effects* | - |
dc.subject.MESH | Muscle, Smooth, Vascular/cytology | - |
dc.subject.MESH | Muscle, Smooth, Vascular/drug effects | - |
dc.subject.MESH | Muscle, Smooth, Vascular/metabolism* | - |
dc.subject.MESH | Myosin-Light-Chain Phosphatase/metabolism | - |
dc.subject.MESH | Phosphorylation | - |
dc.subject.MESH | Phosphorylcholine/analogs & derivatives* | - |
dc.subject.MESH | Phosphorylcholine/metabolism | - |
dc.subject.MESH | Phosphorylcholine/pharmacology | - |
dc.subject.MESH | Rabbits | - |
dc.subject.MESH | Sarcoplasmic Reticulum/metabolism | - |
dc.subject.MESH | Signal Transduction/physiology* | - |
dc.subject.MESH | Sphingosine/analogs & derivatives* | - |
dc.subject.MESH | Sphingosine/metabolism | - |
dc.subject.MESH | Sphingosine/pharmacology | - |
dc.subject.MESH | rho-Associated Kinases/metabolism | - |
dc.title | Comparison of contractile mechanisms of sphingosylphosphorylcholine and sphingosine-1-phosphate in rabbit coronary artery | - |
dc.type | Article | - |
dc.contributor.college | College of Medicine (의과대학) | - |
dc.contributor.department | Dept. of Physiology (생리학) | - |
dc.contributor.googleauthor | Soo-Kyoung Choi | - |
dc.contributor.googleauthor | Duck-Sun Ahn | - |
dc.contributor.googleauthor | Young-Ho Lee | - |
dc.identifier.doi | 10.1093/cvr/cvp054 | - |
dc.admin.author | false | - |
dc.admin.mapping | false | - |
dc.contributor.localId | A02223 | - |
dc.contributor.localId | A02968 | - |
dc.contributor.localId | A04091 | - |
dc.relation.journalcode | J00464 | - |
dc.identifier.eissn | 1755-3245 | - |
dc.identifier.pmid | 19218288 | - |
dc.subject.keyword | Sphingosylphosphorylcholine | - |
dc.subject.keyword | Sphingosine-1-phosphate | - |
dc.subject.keyword | [Ca2+]I | - |
dc.subject.keyword | RhoA/RhoA-associated kinase | - |
dc.subject.keyword | Rabbit coronary artery | - |
dc.contributor.alternativeName | Ahn, Duk Sun | - |
dc.contributor.alternativeName | Lee, Young Ho | - |
dc.contributor.alternativeName | Choi, Soo Kyoung | - |
dc.contributor.affiliatedAuthor | Ahn, Duk Sun | - |
dc.contributor.affiliatedAuthor | Lee, Young Ho | - |
dc.contributor.affiliatedAuthor | Choi, Soo Kyoung | - |
dc.citation.volume | 82 | - |
dc.citation.number | 2 | - |
dc.citation.startPage | 324 | - |
dc.citation.endPage | 332 | - |
dc.identifier.bibliographicCitation | CARDIOVASCULAR RESEARCH, Vol.82(2) : 324-332, 2009 | - |
dc.identifier.rimsid | 36664 | - |
dc.type.rims | ART | - |
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