Article: Effects of triiodo-thyronine on angiotensin-induced cardiomyocyte hypertrophy: Reversal of increased β-myosin heavy chain gene expression

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TitleEffects of triiodo-thyronine on angiotensin-induced cardiomyocyte hypertrophy: Reversal of increased β-myosin heavy chain gene expression
AuthorsWang, B1
Ouyang, J1
Xia, Z2
Issue Date2006
PublisherN R C Research Press. The Journal's web site is located at http://pubs.nrc-cnrc.gc.ca/cgi-bin/rp/rp2_desc_e?cjpp
CitationCanadian Journal Of Physiology And Pharmacology, 2006, v. 84 n. 8-9, p. 935-941 [How to Cite?]
DOI: http://dx.doi.org/10.1139/Y06-043
AbstractThyroid hormone-induced cardiac hypertrophy is similar to that observed in physiological hypertrophy, which is associated with high cardiac contractility and increased α-myosin heavy chain (α-MHC, the high ATPase activity isoform) expression. In contrast, angiotensin II (Ang II) induces an increase in myocardial mass with a compromised contractility accompanied by a shift from oc-MHC to the fetal isoform β-MHC (the low ATPase activity isoform), which is considered as a pathological hypertrophy and inevitably leads to the development of heart failure. The present study is designed to assess the effect of thyroid hormone on angiotensin II-induced hypertrophic growth of cardiomyocytes in vitro. Cardiomyocytes were prepared from hearts of neonatal Wistar rats. The effects of Ang II and 3,3′,5-triiodo-thyronine (T 3) on incorporations of [3H]-thymine and [ 3H]-leucine, MHC isoform mRNA expression, PKC activity, and PKC isoform protein expression were studied. Ang II enhanced [3H]-leucine incorporation, β-MHC mRNA expression, PKC activity, and PKCε expression and inhibited α-MHC mRNA expression in cardiomyocytes. T 3 treatment prevented Ang II-induced increases in PKC activity, PKCε, and β-MHC mRNA overexpression and favored α-MHC mRNA expression. Thyroid hormone appears to be able to reprogram gene expression in Ang II-induced cardiac hypertrophy, and a PKC signal pathway may be involved in such remodeling process. © 2006 NRC Canada.
ISSN0008-4212
2011 Impact Factor: 1.953
2011 SCImago Journal Rankings: 0.149
DOIhttp://dx.doi.org/10.1139/Y06-043
ReferencesReferences in Scopus
DC Field
Value
dc.contributor.authorWang, B
dc.contributor.authorOuyang, J
dc.contributor.authorXia, Z
dc.date.accessioned2012-05-29T06:00:58Z
dc.date.available2012-05-29T06:00:58Z
dc.date.issued2006
dc.description.abstractThyroid hormone-induced cardiac hypertrophy is similar to that observed in physiological hypertrophy, which is associated with high cardiac contractility and increased α-myosin heavy chain (α-MHC, the high ATPase activity isoform) expression. In contrast, angiotensin II (Ang II) induces an increase in myocardial mass with a compromised contractility accompanied by a shift from oc-MHC to the fetal isoform β-MHC (the low ATPase activity isoform), which is considered as a pathological hypertrophy and inevitably leads to the development of heart failure. The present study is designed to assess the effect of thyroid hormone on angiotensin II-induced hypertrophic growth of cardiomyocytes in vitro. Cardiomyocytes were prepared from hearts of neonatal Wistar rats. The effects of Ang II and 3,3′,5-triiodo-thyronine (T 3) on incorporations of [3H]-thymine and [ 3H]-leucine, MHC isoform mRNA expression, PKC activity, and PKC isoform protein expression were studied. Ang II enhanced [3H]-leucine incorporation, β-MHC mRNA expression, PKC activity, and PKCε expression and inhibited α-MHC mRNA expression in cardiomyocytes. T 3 treatment prevented Ang II-induced increases in PKC activity, PKCε, and β-MHC mRNA overexpression and favored α-MHC mRNA expression. Thyroid hormone appears to be able to reprogram gene expression in Ang II-induced cardiac hypertrophy, and a PKC signal pathway may be involved in such remodeling process. © 2006 NRC Canada.
dc.description.natureLink_to_subscribed_fulltext
dc.identifier.citationCanadian Journal Of Physiology And Pharmacology, 2006, v. 84 n. 8-9, p. 935-941 [How to Cite?]
DOI: http://dx.doi.org/10.1139/Y06-043
dc.identifier.doihttp://dx.doi.org/10.1139/Y06-043
dc.identifier.epage941
dc.identifier.isiWOS:000242210800015
dc.identifier.issn0008-4212
2011 Impact Factor: 1.953
2011 SCImago Journal Rankings: 0.149
dc.identifier.issue8-9
dc.identifier.pmid17111039
dc.identifier.scopuseid_2-s2.0-33846447480
dc.identifier.spage935
dc.identifier.urihttp://hdl.handle.net/10722/147239
dc.identifier.volume84
dc.languageeng
dc.publisherN R C Research Press. The Journal's web site is located at http://pubs.nrc-cnrc.gc.ca/cgi-bin/rp/rp2_desc_e?cjpp
dc.publisher.placeCanada
dc.relation.ispartofCanadian Journal of Physiology and Pharmacology
dc.relation.referencesReferences in Scopus
dc.subject.meshAngiotensins
dc.subject.meshAnimals
dc.subject.meshAnimals, Newborn
dc.subject.meshCells, Cultured
dc.subject.meshGene Expression Regulation - Drug Effects
dc.subject.meshHypertrophy - Chemically Induced - Prevention & Control
dc.subject.meshLeucine - Metabolism
dc.subject.meshMyocytes, Cardiac - Drug Effects - Metabolism - Pathology
dc.subject.meshMyosin Heavy Chains - Genetics - Metabolism
dc.subject.meshProtein Isoforms - Genetics - Metabolism
dc.subject.meshProtein Kinase C - Metabolism
dc.subject.meshRna, Messenger - Metabolism
dc.subject.meshRats
dc.subject.meshRats, Wistar
dc.subject.meshThymine - Metabolism
dc.subject.meshTriiodothyronine - Pharmacology
dc.titleEffects of triiodo-thyronine on angiotensin-induced cardiomyocyte hypertrophy: Reversal of increased β-myosin heavy chain gene expression
dc.typeArticle
Author Affiliations
  1. Wuhan University
  2. The University of British Columbia