Quantification of carbonic anhydrase gene expression in ventricle of hypertrophic and failing human heart

Background: Carbonic anhydrase enzymes (CA) catalyze the reversible hydration of carbon dioxide to bicarbonate in mammalian cells. Trans-membrane transport of CA-produced bicarbonate contributes significantly to cellular pH regulation. A body of evidence implicates pH-regulatory processes in the hyp...

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Autores: Alvarez, Bernardo, Quon, Anita L., Mullen, John, Casey, Joseph R.
Formato: artículo
Estado:Versión publicada
Fecha de publicación:2013
País:Argentina
Recursos:Consejo Nacional de Investigaciones Científicas y Técnicas
Repositorio:CONICET Digital (CONICET)
Idioma:inglés
OAI Identifier:oai:ri.conicet.gov.ar:11336/11943
Acesso em linha:http://hdl.handle.net/11336/11943
Access Level:acceso abierto
Palavra-chave:Heart failure
Carbonic anhydrase
pH regulation
Gene expression
Cardiac hypertrophy
https://purl.org/becyt/ford/3.2
https://purl.org/becyt/ford/3
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repository_id_str
dc.title.none.fl_str_mv Quantification of carbonic anhydrase gene expression in ventricle of hypertrophic and failing human heart
title Quantification of carbonic anhydrase gene expression in ventricle of hypertrophic and failing human heart
spellingShingle Quantification of carbonic anhydrase gene expression in ventricle of hypertrophic and failing human heart
Alvarez, Bernardo
Heart failure
Carbonic anhydrase
pH regulation
Gene expression
Cardiac hypertrophy
https://purl.org/becyt/ford/3.2
https://purl.org/becyt/ford/3
title_short Quantification of carbonic anhydrase gene expression in ventricle of hypertrophic and failing human heart
title_full Quantification of carbonic anhydrase gene expression in ventricle of hypertrophic and failing human heart
title_fullStr Quantification of carbonic anhydrase gene expression in ventricle of hypertrophic and failing human heart
title_full_unstemmed Quantification of carbonic anhydrase gene expression in ventricle of hypertrophic and failing human heart
title_sort Quantification of carbonic anhydrase gene expression in ventricle of hypertrophic and failing human heart
dc.creator.none.fl_str_mv Alvarez, Bernardo
Quon, Anita L.
Mullen, John
Casey, Joseph R.
author Alvarez, Bernardo
author_facet Alvarez, Bernardo
Quon, Anita L.
Mullen, John
Casey, Joseph R.
author_role author
author2 Quon, Anita L.
Mullen, John
Casey, Joseph R.
author2_role author
author
author
dc.subject.none.fl_str_mv Heart failure
Carbonic anhydrase
pH regulation
Gene expression
Cardiac hypertrophy
https://purl.org/becyt/ford/3.2
https://purl.org/becyt/ford/3
topic Heart failure
Carbonic anhydrase
pH regulation
Gene expression
Cardiac hypertrophy
https://purl.org/becyt/ford/3.2
https://purl.org/becyt/ford/3
description Background: Carbonic anhydrase enzymes (CA) catalyze the reversible hydration of carbon dioxide to bicarbonate in mammalian cells. Trans-membrane transport of CA-produced bicarbonate contributes significantly to cellular pH regulation. A body of evidence implicates pH-regulatory processes in the hypertrophic growth pathway characteristic of hearts as they fail. In particular, Na+ /H+ exchange (NHE) activation is pro-hypertrophic and CA activity activates NHE. Recently Cardrase (6-ethoxyzolamide), a CA inhibitor, was found to prevent and revert agonist-stimulated cardiac hypertrophy (CH) in cultured cardiomyocytes. Our goal thus was to determine whether hypertrophied human hearts have altered expression of CA isoforms. Methods: We measured CA expression in hypertrophied human hearts to begin to examine the role of carbonic anhydrase in progression of human heart failure. Ventricular biopsies were obtained from patients undergoing cardiac surgery (CS, n = 14), or heart transplantation (HT, n = 13). CS patients presented mild/moderate concentric left ventricular hypertrophy and normal right ventricles, with preserved ventricular function; ejection fractions were ~60%. Conversely, HT patients with failing hearts presented CH or ventricular dilation accompanied by ventricular dysfunction and EF values of 20%. Non-hypertrophic, non-dilated ventricular samples served as controls. Results: Expression of atrial and brain natriuretic peptide (ANP and BNP) were markers of CH. Hypertrophic ventricles presented increased expression of CAII, CAIV, ANP, and BNP, mRNA levels, which increased in failing hearts, measured by quantitative real-time PCR. CAII, CAIV, and ANP protein expression also increased approximately two-fold in hypertrophic/dilated ventricles. Conclusions: These results, combined with in vitro data that CA inhibition prevents and reverts CH, suggest that increased carbonic anhydrase expression is a prognostic molecular marker of cardiac hypertrophy.
publishDate 2013
dc.date.none.fl_str_mv 2013-01
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/11943
Alvarez, Bernardo; Quon, Anita L.; Mullen, John; Casey, Joseph R.; Quantification of carbonic anhydrase gene expression in ventricle of hypertrophic and failing human heart; Biomed Central; Bmc Cardiovascular Disorders; 13; 2; 1-2013; 1-10
1471-2261
url http://hdl.handle.net/11336/11943
identifier_str_mv Alvarez, Bernardo; Quon, Anita L.; Mullen, John; Casey, Joseph R.; Quantification of carbonic anhydrase gene expression in ventricle of hypertrophic and failing human heart; Biomed Central; Bmc Cardiovascular Disorders; 13; 2; 1-2013; 1-10
1471-2261
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/doi/10.1186/1471-2261-13-2
info:eu-repo/semantics/altIdentifier/url/http://bmccardiovascdisord.biomedcentral.com/articles/10.1186/1471-2261-13-2
info:eu-repo/semantics/altIdentifier/url/https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3570296/
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
application/pdf
dc.publisher.none.fl_str_mv Biomed Central
publisher.none.fl_str_mv Biomed Central
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
repository.name.fl_str_mv CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
_version_ 1799195230277206016
spelling Quantification of carbonic anhydrase gene expression in ventricle of hypertrophic and failing human heartAlvarez, BernardoQuon, Anita L.Mullen, JohnCasey, Joseph R.Heart failureCarbonic anhydrasepH regulationGene expressionCardiac hypertrophyhttps://purl.org/becyt/ford/3.2https://purl.org/becyt/ford/3Background: Carbonic anhydrase enzymes (CA) catalyze the reversible hydration of carbon dioxide to bicarbonate in mammalian cells. Trans-membrane transport of CA-produced bicarbonate contributes significantly to cellular pH regulation. A body of evidence implicates pH-regulatory processes in the hypertrophic growth pathway characteristic of hearts as they fail. In particular, Na+ /H+ exchange (NHE) activation is pro-hypertrophic and CA activity activates NHE. Recently Cardrase (6-ethoxyzolamide), a CA inhibitor, was found to prevent and revert agonist-stimulated cardiac hypertrophy (CH) in cultured cardiomyocytes. Our goal thus was to determine whether hypertrophied human hearts have altered expression of CA isoforms. Methods: We measured CA expression in hypertrophied human hearts to begin to examine the role of carbonic anhydrase in progression of human heart failure. Ventricular biopsies were obtained from patients undergoing cardiac surgery (CS, n = 14), or heart transplantation (HT, n = 13). CS patients presented mild/moderate concentric left ventricular hypertrophy and normal right ventricles, with preserved ventricular function; ejection fractions were ~60%. Conversely, HT patients with failing hearts presented CH or ventricular dilation accompanied by ventricular dysfunction and EF values of 20%. Non-hypertrophic, non-dilated ventricular samples served as controls. Results: Expression of atrial and brain natriuretic peptide (ANP and BNP) were markers of CH. Hypertrophic ventricles presented increased expression of CAII, CAIV, ANP, and BNP, mRNA levels, which increased in failing hearts, measured by quantitative real-time PCR. CAII, CAIV, and ANP protein expression also increased approximately two-fold in hypertrophic/dilated ventricles. Conclusions: These results, combined with in vitro data that CA inhibition prevents and reverts CH, suggest that increased carbonic anhydrase expression is a prognostic molecular marker of cardiac hypertrophy.Fil: Alvarez, Bernardo. Universidad Nacional de la Plata. Facultad de Ciencias Médicas; Argentina. Consejo Nacional de Investigaciones Cientificas y Tecnicas. Centro Cientifico Tecnológico La Plata. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani"; ArgentinaFil: Quon, Anita L.. University Of Alberta. Faculty Of Medicine And Oral Health Sciences; CanadáFil: Mullen, John. University of Alberta; CanadáFil: Casey, Joseph R.. University Of Alberta. Faculty Of Medicine And Oral Health Sciences; CanadáBiomed Central2013-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/11943Alvarez, Bernardo; Quon, Anita L.; Mullen, John; Casey, Joseph R.; Quantification of carbonic anhydrase gene expression in ventricle of hypertrophic and failing human heart; Biomed Central; Bmc Cardiovascular Disorders; 13; 2; 1-2013; 1-101471-2261enginfo:eu-repo/semantics/altIdentifier/doi/10.1186/1471-2261-13-2info:eu-repo/semantics/altIdentifier/url/http://bmccardiovascdisord.biomedcentral.com/articles/10.1186/1471-2261-13-2info:eu-repo/semantics/altIdentifier/url/https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3570296/info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2024-05-08T13:46:44Zoai:ri.conicet.gov.ar:11336/11943instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982024-05-08 13:46:44.447CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
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