STIM1 silencing prevents pressure-overload induced cardiac hypertrophy in mice
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Benard, Ludovic Olivier | - |
dc.contributor.author | Jeong, Dongtak | - |
dc.contributor.author | Matasic, Daniel S. | - |
dc.contributor.author | Kohlbrenner, Erik | - |
dc.contributor.author | Hajjar, Roger J. | - |
dc.contributor.author | Hulot, Jean-Sebastien | - |
dc.date.accessioned | 2021-06-23T07:52:50Z | - |
dc.date.available | 2021-06-23T07:52:50Z | - |
dc.date.issued | 2012-04 | - |
dc.identifier.issn | 0892-6638 | - |
dc.identifier.issn | 1530-6860 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/erica/handle/2021.sw.erica/33151 | - |
dc.description.abstract | STromal Interaction Molecule 1 (STIM1), a membrane protein of the endoplasmic reticulum (ER), has recently been proposed as a positive regulator of cardiomyocyte growth by promoting calcium (Ca2+) entry through the plasma membrane and the activation of Ca2+-mediated signaling pathways (Circulation, 2011). To further extend this observation, we studied the impact of STIM1 silencing in pressure-overload induced mouse model of cardiac hypertrophy using recombinant Associated Adenovirus 9 (AAV9)-mediated gene silencing. C57/Bl6 Mice were injected with saline (noAAV) or with rAAV9 expressing shRNA against STIM1 (shSTIM1) or a control shRNA (shScr) at 1E+11 viral genome by tail vein injection. Three weeks later, Transverse Aortic Constriction (TAC) surgery was performed (4 experimental groups: sham, TAC-noAAV, TAC-shScr and TAC-shSTIM1). In contrast to TAC-noAAV or TAC-shScr, the rAAV9-shSTIM1 treated animals developed significantly reduced cardiac hypertrophy developed as assessed by echocardiogtaphy and hemodynamics three weeks after surgery. TAC-ShSTIM1 however displayed left ventricular dilation and a non-significant trend for depressed systolic function. These results indicate STIM1 as a key regulator of cardiac hypertrophy. | - |
dc.language | 영어 | - |
dc.language.iso | ENG | - |
dc.publisher | Federation of American Societies for Experimental Biology | - |
dc.title | STIM1 silencing prevents pressure-overload induced cardiac hypertrophy in mice | - |
dc.type | Article | - |
dc.publisher.location | 미국 | - |
dc.identifier.doi | 10.1096/fasebj.26.1_supplement.137.7 | - |
dc.identifier.wosid | 000310711305049 | - |
dc.identifier.bibliographicCitation | FASEB Journal, v.26 | - |
dc.citation.title | FASEB Journal | - |
dc.citation.volume | 26 | - |
dc.type.docType | Meeting Abstract | - |
dc.description.isOpenAccess | N | - |
dc.description.journalRegisteredClass | sci | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Biochemistry & Molecular Biology | - |
dc.relation.journalResearchArea | Life Sciences & Biomedicine - Other Topics | - |
dc.relation.journalResearchArea | Cell Biology | - |
dc.relation.journalWebOfScienceCategory | Biochemistry & Molecular Biology | - |
dc.relation.journalWebOfScienceCategory | Biology | - |
dc.relation.journalWebOfScienceCategory | Cell Biology | - |
dc.identifier.url | https://faseb.onlinelibrary.wiley.com/doi/abs/10.1096%2Ffasebj.26.1_supplement.137.7 | - |
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.
55 Hanyangdeahak-ro, Sangnok-gu, Ansan, Gyeonggi-do, 15588, Korea+82-31-400-4269 sweetbrain@hanyang.ac.kr
COPYRIGHT © 2021 HANYANG UNIVERSITY. ALL RIGHTS RESERVED.
Certain data included herein are derived from the © Web of Science of Clarivate Analytics. All rights reserved.
You may not copy or re-distribute this material in whole or in part without the prior written consent of Clarivate Analytics.