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MicroRNA-145 suppresses ROS-induced Ca2+ overload of cardiomyocytes by targeting CaMKIIδ

DC FieldValueLanguage
dc.contributor.author이창연-
dc.contributor.author차민지-
dc.contributor.author최은미-
dc.contributor.author최은현-
dc.contributor.author함온주-
dc.contributor.author황기철-
dc.contributor.author황혜진-
dc.contributor.author박준희-
dc.contributor.author서향희-
dc.contributor.author송병욱-
dc.contributor.author이세연-
dc.contributor.author이지윤-
dc.date.accessioned2014-12-18T08:45:37Z-
dc.date.available2014-12-18T08:45:37Z-
dc.date.issued2013-
dc.identifier.issn0006-291X-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/86902-
dc.description.abstractA change in intracellular free calcium (Ca(2+)) is a common signaling mechanism of reperfusion-induced cardiomyocyte death. Calcium/calmodulin dependent protein kinase II (CaMKII) is a critical regulator of Ca(2+) signaling and mediates signaling pathways responsible for functions in the heart including hypertrophy, apoptosis, arrhythmia, and heart disease. MicroRNAs (miRNA) are involved in the regulation of cell response, including survival, proliferation, apoptosis, and development. However, the roles of miRNAs in Ca(2+)-mediated apoptosis of cardiomyocytes are uncertain. Here, we determined the potential role of miRNA in the regulation of CaMKII dependent apoptosis and explored its underlying mechanism. To determine the potential roles of miRNAs in H2O2-mediated Ca(2+) overload, we selected and tested 6 putative miRNAs that targeted CaMKIIδ, and showed that miR-145 represses CaMKIIδ protein expression and Ca(2+) overload. We confirmed CaMKIIδ as a direct downstream target of miR-145. Furthermore, miR-145 regulates Ca(2+)-related signals and ameliorates apoptosis. This study demonstrates that miR-145 regulates reactive oxygen species (ROS)-induced Ca(2+) overload in cardiomyocytes. Thus, miR-145 affects ROS-mediated gene regulation and cellular injury responses.-
dc.description.statementOfResponsibilityopen-
dc.relation.isPartOfBIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS-
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.MESHAnimals, Newborn-
dc.subject.MESHCalcium/metabolism*-
dc.subject.MESHCalcium-Calmodulin-Dependent Protein Kinase Type 2/metabolism*-
dc.subject.MESHCells, Cultured-
dc.subject.MESHHydrogen Peroxide/metabolism*-
dc.subject.MESHMicroRNAs/pharmacology*-
dc.subject.MESHMyocytes, Cardiac/drug effects-
dc.subject.MESHMyocytes, Cardiac/metabolism*-
dc.subject.MESHRats-
dc.subject.MESHRats, Sprague-Dawley-
dc.subject.MESHReactive Oxygen Species/metabolism*-
dc.titleMicroRNA-145 suppresses ROS-induced Ca2+ overload of cardiomyocytes by targeting CaMKIIδ-
dc.typeArticle-
dc.contributor.collegeResearcher Institutes (부설 연구소)-
dc.contributor.departmentYonsei Integrative Research Institute for Cerebral & Cardiovascular Disease (뇌심혈관질환융합연구사업단)-
dc.contributor.googleauthorMin-Ji Cha-
dc.contributor.googleauthorJin-Kyung Jang-
dc.contributor.googleauthorOnju Ham-
dc.contributor.googleauthorByeong-Wook Song-
dc.contributor.googleauthorSe-Yeon Lee-
dc.contributor.googleauthorChang Yeon Lee-
dc.contributor.googleauthorJun-Hee Park-
dc.contributor.googleauthorJiyun Lee-
dc.contributor.googleauthorHyang-Hee Seo-
dc.contributor.googleauthorEunhyun Choi-
dc.contributor.googleauthorWoo-min Jeon-
dc.contributor.googleauthorHye Jin Hwang-
dc.contributor.googleauthorHyun-Taek Shin-
dc.contributor.googleauthorEunmi Choi-
dc.contributor.googleauthorKi-Chul Hwang-
dc.identifier.doi10.1016/j.bbrc.2013.05.050-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA03244-
dc.contributor.localIdA03995-
dc.contributor.localIdA04162-
dc.contributor.localIdA04336-
dc.contributor.localIdA04456-
dc.contributor.localIdA04496-
dc.contributor.localIdA01679-
dc.contributor.localIdA01921-
dc.contributor.localIdA02026-
dc.contributor.localIdA02880-
dc.contributor.localIdA03208-
dc.contributor.localIdA04151-
dc.relation.journalcodeJ00281-
dc.identifier.eissn1090-2104-
dc.identifier.pmid23702479-
dc.identifier.urlhttp://www.sciencedirect.com/science/article/pii/S0006291X13008334-
dc.subject.keywordMicroRNA-145-
dc.subject.keywordCardiomyocytes-
dc.subject.keywordCalcium overload-
dc.subject.keywordCalcium/calmodulin dependent protein kinase Iiδ-
dc.subject.keywordApoptosis-
dc.contributor.alternativeNameLee, Chang Yeon-
dc.contributor.alternativeNameCha, Min Ji-
dc.contributor.alternativeNameChoi, Eun Mi-
dc.contributor.alternativeNameChoi, Eun Hyun-
dc.contributor.alternativeNameHam, On Ju-
dc.contributor.alternativeNameHwang, Ki Chul-
dc.contributor.alternativeNameHwang, Hye Jin-
dc.contributor.alternativeNamePark, Jun-Hee-
dc.contributor.alternativeNameSeo, Hyang Hee-
dc.contributor.alternativeNameSong, Byeong Wook-
dc.contributor.alternativeNameLee, Se Yeon-
dc.contributor.alternativeNameLee, Ji Yun-
dc.contributor.affiliatedAuthorLee, Chang Yeon-
dc.contributor.affiliatedAuthorCha, Min Ji-
dc.contributor.affiliatedAuthorChoi, Eun Hyun-
dc.contributor.affiliatedAuthorHam, On Ju-
dc.contributor.affiliatedAuthorHwang, Ki Chul-
dc.contributor.affiliatedAuthorHwang, Hye Jin-
dc.contributor.affiliatedAuthorPark, Jun-Hee-
dc.contributor.affiliatedAuthorSeo, Hyang Hee-
dc.contributor.affiliatedAuthorSong, Byeong Wook-
dc.contributor.affiliatedAuthorLee, Se Yeon-
dc.contributor.affiliatedAuthorLee, Ji Yun-
dc.contributor.affiliatedAuthorChoi, Eun Mi-
dc.rights.accessRightsnot free-
dc.citation.volume435-
dc.citation.number4-
dc.citation.startPage720-
dc.citation.endPage726-
dc.identifier.bibliographicCitationBIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, Vol.435(4) : 720-726, 2013-
Appears in Collections:
5. Research Institutes (연구소) > Yonsei Integrative Research Institute for Cerebral & Cardiovascular Disease (뇌심혈관질환융합연구사업단) > 1. Journal Papers
1. College of Medicine (의과대학) > Yonsei Biomedical Research Center (연세의생명연구원) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > BioMedical Science Institute (의생명과학부) > 1. Journal Papers

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