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dc.rights.licenseopenen_US
dc.contributor.authorABDULRAHMAN, Nabeel
hal.structure.identifierBiologie des maladies cardiovasculaires = Biology of Cardiovascular Diseases
dc.contributor.authorJASPARD-VINASSA, Beatrice
dc.contributor.authorFLIEGEL, Larry
dc.contributor.authorJABEEN, Aayesha
dc.contributor.authorRIAZ, Sadaf
hal.structure.identifierBiologie des maladies cardiovasculaires = Biology of Cardiovascular Diseases
dc.contributor.authorGADEAU, Alain-Pierre
dc.contributor.authorMRAICHE, Fatima
dc.date.accessioned2023-01-16T14:48:48Z
dc.date.available2023-01-16T14:48:48Z
dc.date.issued2018-05-01
dc.identifier.issn1531-2267en_US
dc.identifier.urihttps://oskar-bordeaux.fr/handle/20.500.12278/171690
dc.description.abstractEnCardiovascular diseases are the leading cause of death worldwide. One in three cases of heart failure is due to dilated cardiomyopathy. The Na/H exchanger isoform 1 (NHE1), a multifunctional protein and the key pH regulator in the heart, has been demonstrated to be increased in this condition. We have previously demonstrated that elevated NHE1 activity induced cardiac hypertrophy in vivo. Furthermore, the overexpression of active NHE1 elicited modulation of gene expression in cardiomyocytes including an upregulation of myocardial osteopontin (OPN) expression. To determine the role of OPN in inducing NHE1-mediated cardiomyocyte hypertrophy, double transgenic mice expressing active NHE1 and OPN knockout were generated and assessed by echocardiography and the cardiac phenotype. Our studies showed that hearts expressing active NHE1 exhibited cardiac remodeling indicated by increased systolic and diastolic left ventricular internal diameter and increased ventricular volume. Moreover, these hearts demonstrated impaired function with decreased fractional shortening and ejection fraction. Atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) mRNA was upregulated, and there was an increase in heart cell cross-sectional area confirming the cardiac hypertrophic effect. Moreover, NHE1 transgenic mice also showed increased collagen deposition, upregulation of CD44 and phosphorylation of p90 ribosomal s6 kinase (RSK), effects that were regressed in OPN knockout mice. In conclusion, we developed an interesting comparative model of active NHE1 transgenic mouse lines which express a dilated hypertrophic phenotype expressing CD44 and phosphorylated RSK, effects which were regressed in absence of OPN.
dc.language.isoENen_US
dc.subject.enAnimals
dc.subject.enCardiomegaly
dc.subject.enGene Expression Regulation
dc.subject.enHyaluronan Receptors
dc.subject.enMice
dc.subject.enKnockout
dc.subject.enMice
dc.subject.enTransgenic
dc.subject.enMyocardium
dc.subject.enMyocytes
dc.subject.enCardiac
dc.subject.enOsteopontin
dc.subject.enPhosphorylation
dc.subject.enRibosomal Protein S6 Kinases
dc.subject.en90-kDa
dc.subject.enSodium-Hydrogen Exchanger 1
dc.title.enNa/H exchanger isoform 1-induced osteopontin expression facilitates cardiac hypertrophy through p90 ribosomal S6 kinase.
dc.title.alternativePhysiol Genomicsen_US
dc.typeArticle de revueen_US
dc.identifier.doi10.1152/physiolgenomics.00133.2017en_US
dc.subject.halSciences du Vivant [q-bio]/Médecine humaine et pathologieen_US
dc.identifier.pubmed29473817en_US
bordeaux.journalPhysiological Genomicsen_US
bordeaux.page332-342en_US
bordeaux.volume50en_US
bordeaux.hal.laboratoriesBiologie des maladies cardiovasculaires (BMC) - UMR 1034en_US
bordeaux.issue5en_US
bordeaux.institutionUniversité de Bordeauxen_US
bordeaux.institutionINSERMen_US
bordeaux.peerReviewedouien_US
bordeaux.inpressnonen_US
bordeaux.import.sourcepubmed
hal.exportfalse
workflow.import.sourcepubmed
dc.rights.ccPas de Licence CCen_US
bordeaux.COinSctx_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.jtitle=Physiological%20Genomics&rft.date=2018-05-01&rft.volume=50&rft.issue=5&rft.spage=332-342&rft.epage=332-342&rft.eissn=1531-2267&rft.issn=1531-2267&rft.au=ABDULRAHMAN,%20Nabeel&JASPARD-VINASSA,%20Beatrice&FLIEGEL,%20Larry&JABEEN,%20Aayesha&RIAZ,%20Sadaf&rft.genre=article


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