Cited 12 times in
Protective Effect of Peroxisome Proliferator-Activated Receptor α Activation against Cardiac Ischemia-Reperfusion Injury Is Related to Upregulation of Uncoupling Protein-3
DC Field | Value | Language |
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dc.contributor.author | 곽영란 | - |
dc.contributor.author | 김재우 | - |
dc.contributor.author | 김효정 | - |
dc.contributor.author | 송종욱 | - |
dc.date.accessioned | 2017-02-24T03:11:41Z | - |
dc.date.available | 2017-02-24T03:11:41Z | - |
dc.date.issued | 2016 | - |
dc.identifier.issn | 1942-0900 | - |
dc.identifier.uri | https://ir.ymlib.yonsei.ac.kr/handle/22282913/146274 | - |
dc.description.abstract | Activation of peroxisome proliferator-activated receptor α (PPARα) confers cardioprotection, while its mechanism remains elusive. We investigated the protective effect of PPARα activation against cardiac ischemia-reperfusion injury in terms of the expression of uncoupling protein (UCP). Myocardial infarct size and UCP expression were measured in rats treated with WY-14643 20 mg/kg, a PPARα ligand, or vehicle. WY-14643 increased UCP3 expression in vivo. Myocardial infarct size was decreased in the WY-14643 group (76 ± 8% versus 42 ± 12%, P<0.05). During reperfusion, the incidence of arrhythmia was higher in the control group compared with the WY-14643 group (9/10 versus 3/10, P<0.05). H9c2 cells were incubated for 24 h with WY-14643 or vehicle. WY-14643 increased UCP3 expression in H9c2 cells. WY-14643 decreased hypoxia-stimulated ROS production. Cells treated with WY-14643 were more resistant to hypoxia-reoxygenation than the untreated cells. Knocking-down UCP3 by siRNA prevented WY-14643 from attenuating the production of ROS. UCP3 siRNA abolished the effect of WY-14643 on cell viability against hypoxia-reoxygenation. In summary, administration of PPARα agonist WY-14643 mitigated the extent of myocardial infarction and incidence of reperfusion-induced arrhythmia. PPARα activation conferred cytoprotective effect against hypoxia-reoxygenation. Associated mechanisms involved increased UCP3 expression and resultant attenuation of ROS production. | - |
dc.description.statementOfResponsibility | open | - |
dc.format | application/pdf | - |
dc.language | English | - |
dc.publisher | Hindawi Pub. Corp. | - |
dc.relation.isPartOf | OXIDATIVE MEDICINE AND CELLULAR LONGEVITY | - |
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 | Arrhythmias, Cardiac/complications | - |
dc.subject.MESH | Arrhythmias, Cardiac/pathology | - |
dc.subject.MESH | Arrhythmias, Cardiac/physiopathology | - |
dc.subject.MESH | Cardiotonic Agents/metabolism* | - |
dc.subject.MESH | Cell Hypoxia/drug effects | - |
dc.subject.MESH | Cell Line | - |
dc.subject.MESH | Cell Survival/drug effects | - |
dc.subject.MESH | Coronary Occlusion/complications | - |
dc.subject.MESH | Coronary Occlusion/pathology | - |
dc.subject.MESH | Coronary Occlusion/physiopathology | - |
dc.subject.MESH | Coronary Vessels/pathology | - |
dc.subject.MESH | Hemodynamics/drug effects | - |
dc.subject.MESH | Ion Channels/metabolism* | - |
dc.subject.MESH | Male | - |
dc.subject.MESH | Mitochondrial Proteins/metabolism* | - |
dc.subject.MESH | Myocardial Infarction/complications | - |
dc.subject.MESH | Myocardial Infarction/pathology | - |
dc.subject.MESH | Myocardial Infarction/physiopathology | - |
dc.subject.MESH | Myocardial Reperfusion Injury/metabolism* | - |
dc.subject.MESH | Myocardial Reperfusion Injury/pathology* | - |
dc.subject.MESH | Myocardial Reperfusion Injury/physiopathology | - |
dc.subject.MESH | PPAR alpha/metabolism* | - |
dc.subject.MESH | Pyrimidines/pharmacology | - |
dc.subject.MESH | Rats, Sprague-Dawley | - |
dc.subject.MESH | Reactive Oxygen Species/metabolism | - |
dc.subject.MESH | Uncoupling Protein 3 | - |
dc.subject.MESH | Up-Regulation*/drug effects | - |
dc.title | Protective Effect of Peroxisome Proliferator-Activated Receptor α Activation against Cardiac Ischemia-Reperfusion Injury Is Related to Upregulation of Uncoupling Protein-3 | - |
dc.type | Article | - |
dc.publisher.location | United States | - |
dc.contributor.college | College of Medicine | - |
dc.contributor.department | Dept. of Anesthesiology and Pain Medicine | - |
dc.contributor.googleauthor | Jong Wook Song | - |
dc.contributor.googleauthor | Hyo Jung Kim | - |
dc.contributor.googleauthor | Hyelin Lee | - |
dc.contributor.googleauthor | Jae-woo Kim | - |
dc.contributor.googleauthor | Young-Lan Kwak | - |
dc.identifier.doi | 10.1155/2016/3539649 | - |
dc.contributor.localId | A00172 | - |
dc.contributor.localId | A00865 | - |
dc.contributor.localId | A01204 | - |
dc.contributor.localId | A02060 | - |
dc.relation.journalcode | J02455 | - |
dc.identifier.eissn | 1942-0994 | - |
dc.identifier.pmid | 26770648 | - |
dc.contributor.alternativeName | Kwak, Young Lan | - |
dc.contributor.alternativeName | Kim, Jae Woo | - |
dc.contributor.alternativeName | Kim, Hyo Jung | - |
dc.contributor.alternativeName | Song, Jong Wook | - |
dc.contributor.affiliatedAuthor | Kwak, Young Lan | - |
dc.contributor.affiliatedAuthor | Kim, Jae Woo | - |
dc.contributor.affiliatedAuthor | Kim, Hyo Jung | - |
dc.contributor.affiliatedAuthor | Song, Jong Wook | - |
dc.citation.volume | 2016 | - |
dc.citation.startPage | 3539649 | - |
dc.identifier.bibliographicCitation | OXIDATIVE MEDICINE AND CELLULAR LONGEVITY, Vol.2016 : 3539649, 2016 | - |
dc.date.modified | 2017-02-24 | - |
dc.identifier.rimsid | 51327 | - |
dc.type.rims | ART | - |
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