Cited 2 times in
PLCδ1 Protein Rescues Ischemia-reperfused Heart by the Regulation of Calcium Homeostasis
DC Field | Value | Language |
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dc.contributor.author | 이세연 | - |
dc.contributor.author | 이창연 | - |
dc.contributor.author | 임소연 | - |
dc.contributor.author | 장양수 | - |
dc.contributor.author | 함온주 | - |
dc.contributor.author | 황기철 | - |
dc.contributor.author | 박준희 | - |
dc.date.accessioned | 2015-01-06T16:47:54Z | - |
dc.date.available | 2015-01-06T16:47:54Z | - |
dc.date.issued | 2014 | - |
dc.identifier.issn | 1525-0016 | - |
dc.identifier.uri | https://ir.ymlib.yonsei.ac.kr/handle/22282913/98789 | - |
dc.description.abstract | Myocardial Ca2+ overload induced by ischemia/reperfusion (I/R) is a major element of myocardial dysfunction in heart failure. Phospholipase C (PLC) plays important roles in the regulation of the phosphoinositol pathway and Ca2+ homeostasis in various types of cells. Here, we investigated the protective role of PLCδ1 against myocardial I/R injury through the regulation of Ca2+ homeostasis. To investigate its role, PLCδ1 was fused to Hph1, a cell-permeable protein transduction domain (PTD), and treated into rat neonatal cardiomyocytes and rat hearts under respective hypoxia-reoxygenation (H/R) and ischemia-reperfusion conditions. Treatment with Hph1-PLCδ1 significantly inhibited intracellular Ca2+ overload, reactive oxygen species generation, mitochondrial permeability transition pore opening, and mitochondrial membrane potential elevation in H/R neonatal cardiomyocytes, resulting in the inhibition of apoptosis. Intravenous injections of Hph1-PLCδ1 in rats with I/R-injured myocardium caused significant reductions in infarct size and apoptosis and also improved systolic and diastolic cardiac functioning. Furthermore, a small ions profile obtained using time-of-flight secondary ion mass spectrometry showed that treatment with Hph1-PLCδ1 leads to significant recovery of calcium-related ions toward normal levels in I/R-injured myocardium. These results suggest that Hph1-PLCδ1 may manifest as a promising cardioprotective drug due to its inhibition of the mitochondrial apoptotic pathway in cells suffering from I/R injury. | - |
dc.description.statementOfResponsibility | open | - |
dc.format.extent | 1110~1121 | - |
dc.relation.isPartOf | MOLECULAR THERAPY | - |
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 | Animals, Newborn | - |
dc.subject.MESH | Apoptosis/drug effects | - |
dc.subject.MESH | Calcium/metabolism* | - |
dc.subject.MESH | Cell Hypoxia/drug effects | - |
dc.subject.MESH | Injections | - |
dc.subject.MESH | Membrane Potential, Mitochondrial/drug effects | - |
dc.subject.MESH | Mitochondrial Membrane Transport Proteins/drug effects | - |
dc.subject.MESH | Myocardial Reperfusion Injury/drug therapy | - |
dc.subject.MESH | Myocardial Reperfusion Injury/physiopathology* | - |
dc.subject.MESH | Myocytes, Cardiac/drug effects | - |
dc.subject.MESH | Myocytes, Cardiac/pathology | - |
dc.subject.MESH | Phospholipase C gamma/administration & dosage* | - |
dc.subject.MESH | Phospholipase C gamma/genetics | - |
dc.subject.MESH | Phospholipase C gamma/metabolism | - |
dc.subject.MESH | Polycomb Repressive Complex 1/genetics | - |
dc.subject.MESH | Polycomb Repressive Complex 1/metabolism | - |
dc.subject.MESH | Rats | - |
dc.subject.MESH | Rats, Sprague-Dawley | - |
dc.subject.MESH | Reactive Oxygen Species/metabolism | - |
dc.subject.MESH | Recombinant Fusion Proteins/administration & dosage | - |
dc.title | PLCδ1 Protein Rescues Ischemia-reperfused Heart by the Regulation of Calcium Homeostasis | - |
dc.type | Article | - |
dc.contributor.college | Researcher Institutes (부설 연구소) | - |
dc.contributor.department | Yonsei Integrative Research Institute for Cerebral & Cardiovascular Disease (뇌심혈관질환융합연구사업단) | - |
dc.contributor.googleauthor | Soyeon Lim | - |
dc.contributor.googleauthor | Woochul Chang | - |
dc.contributor.googleauthor | Min-Ji Cha | - |
dc.contributor.googleauthor | Byeong-Wook Song | - |
dc.contributor.googleauthor | Onju Ham | - |
dc.contributor.googleauthor | Se-Yeon Lee | - |
dc.contributor.googleauthor | Changyoun Lee | - |
dc.contributor.googleauthor | Jun-Hee Park | - |
dc.contributor.googleauthor | Sang-Kyou Lee | - |
dc.contributor.googleauthor | Yangsoo Jang | - |
dc.contributor.googleauthor | Ki-Chul Hwang | - |
dc.identifier.doi | 10.1038/mt.2014.46 | - |
dc.admin.author | false | - |
dc.admin.mapping | false | - |
dc.contributor.localId | A02880 | - |
dc.contributor.localId | A03244 | - |
dc.contributor.localId | A03448 | - |
dc.contributor.localId | A04336 | - |
dc.contributor.localId | A04456 | - |
dc.contributor.localId | A01679 | - |
dc.contributor.localId | A03373-1 | - |
dc.relation.journalcode | J02271 | - |
dc.identifier.eissn | 1525-0024 | - |
dc.identifier.pmid | 24637455 | - |
dc.identifier.url | http://www.nature.com/mt/journal/v22/n6/full/mt201446a.html | - |
dc.contributor.alternativeName | Lee, Se Yeon | - |
dc.contributor.alternativeName | Lee, Chang Yeon | - |
dc.contributor.alternativeName | Lim, So Yeon | - |
dc.contributor.alternativeName | Jang, Yang Soo | - |
dc.contributor.alternativeName | Ham, On Ju | - |
dc.contributor.alternativeName | Hwang, Ki Chul | - |
dc.contributor.alternativeName | Park, Jun-Hee | - |
dc.contributor.affiliatedAuthor | Lee, Se Yeon | - |
dc.contributor.affiliatedAuthor | Lee, Chang Yeon | - |
dc.contributor.affiliatedAuthor | Jang, Yang Soo | - |
dc.contributor.affiliatedAuthor | Ham, On Ju | - |
dc.contributor.affiliatedAuthor | Hwang, Ki Chul | - |
dc.contributor.affiliatedAuthor | Park, Jun-Hee | - |
dc.contributor.affiliatedAuthor | Lim, So Yeon | - |
dc.rights.accessRights | free | - |
dc.citation.volume | 22 | - |
dc.citation.number | 6 | - |
dc.citation.startPage | 1110 | - |
dc.citation.endPage | 1121 | - |
dc.identifier.bibliographicCitation | MOLECULAR THERAPY, Vol.22(6) : 1110-1121, 2014 | - |
dc.identifier.rimsid | 39246 | - |
dc.type.rims | ART | - |
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