Gene profiling of left ventricle eccentric hypertrophy in aortic regurgitation in rats : rationale for targeting the β-adrenergic and renin-angiotensin systems

DC FieldValueLanguage
dc.contributor.authorChampetier, Serge-
dc.contributor.authorBojmehrani, Azadeh-
dc.contributor.authorBeaudoin, Jonathan-
dc.contributor.authorLachance, Dominic-
dc.contributor.authorPlante, Éric-
dc.contributor.authorRoussel, Élise-
dc.contributor.authorCouët, Jacques-
dc.contributor.authorArsenault, Marie-
dc.date.accessioned2017-11-14T18:56:53Z-
dc.date.available2017-11-14T18:56:53Z-
dc.date.issued2009-03-01-
dc.identifier.issn0363-6135fr
dc.identifier.urihttp://hdl.handle.net/20.500.11794/15829-
dc.description.abstractAortic valve regurgitation (AR) imposes a severe volume overload to the left ventricle (LV), which results in dilation, eccentric hypertrophy, and eventually loss of function. Little is known about the impact of AR on LV gene expression. We, therefore, conducted a gene expression profiling study in the LV of rats with acute and severe AR. We identified 64 genes that were specifically upregulated and 29 that were downregulated out of 21,910 genes after 2 wk. Of the upregulated genes, a good proportion was related to the extracellular matrix. We subsequently studied a subset of 19 genes by quantitative RT-PCR (qRT-PCR) to see if the modulation seen in the LV after 2 wk persisted in the chronic phase (after 6 and 12 mo) and found that it did persist. Knowing that the adrenergic and renin-angiotensin systems are overactivated in our animal model, we were interested to see if blocking those systems using metoprolol (25 mg·kg−1·day−1) and captopril (100 mg·kg−1·day−1) would alter the expression of some upregulated LV genes in AR rats after 6 mo. By qRT-PCR, we observed that upregulations of LV mRNA levels encoding for procollagens type I and III, fibronectin, atrial natriuretic peptide, transforming growth factor-β2, and connective tissue growth factor were totally or partially reversed by this treatment. These observations provide a molecular rationale for a medical strategy aiming these systems in the medical treatment of AR and expand the paradigm in the study of this form of LV volume overload.fr
dc.languageengfr
dc.publisherAmerican Physiological Societyfr
dc.subjectAortic regurgitationfr
dc.subjectHeart hypertrophyfr
dc.subjectVolume overloadfr
dc.subjectGene expressionfr
dc.subjectRenin-angiotensin systemfr
dc.subjectAdrenergic systemfr
dc.titleGene profiling of left ventricle eccentric hypertrophy in aortic regurgitation in rats : rationale for targeting the β-adrenergic and renin-angiotensin systemsfr
dc.title.alternativeGene profiling in volume-overload LV hypertrophyfr
dc.typeCOAR1_1::Texte::Périodique::Revue::Contribution à un journal::Article::Article de recherchefr
dcterms.bibliographicCitationAmerican journal of physiology. Heart and circulatory physiology, Vol. 296 (3), H669-H677 (2009)fr
dc.identifier.doi10.1152/ajpheart.01046.2008fr
dc.identifier.pubmed19112094fr
dc.subject.rvmCœur -- Ventricule gauche -- Hypertrophiefr
dc.subject.rvmExpression géniquefr
dc.subject.rvmRats (Animaux de laboratoire)fr
dc.subject.rvmSystèmes adrénergiquesfr
dc.subject.rvmSystème rénine-angiotensinefr
dc.subject.rvmCœur -- Valvules -- Maladiesfr
rioxxterms.versionAccepted Manuscriptfr
rioxxterms.version_of_recordhttps://doi.org/10.1152/ajpheart.01046.2008fr
rioxxterms.project.funder_nameCanadian Institutes of Health Researchfr
rioxxterms.project.funder_nameCanadian Heart and Stroke Foundationfr
rioxxterms.project.funder_nameQuebec Heart Institute Corporationfr
bul.rights.periodeEmbargo12 moisfr
Collection:Articles publiés dans des revues avec comité de lecture

Files in this item:
Description SizeFormat 
3.pdf462.03 kBAdobe PDFThumbnail
View/Open
Figures.pdf845.21 kBAdobe PDFThumbnail
View/Open
All documents in CorpusUL are protected by Copyright Act of Canada.