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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
2012 Impact Factor: 1.556
2012 SCImago Journal Rankings: 0.550
 
DOIhttp://dx.doi.org/10.1139/Y06-043
 
ISI Accession Number IDWOS:000242210800015
 
ReferencesReferences in Scopus
 
DC FieldValue
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
2012 Impact Factor: 1.556
2012 SCImago Journal Rankings: 0.550
 
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
 
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<description.abstract>Thyroid hormone-induced cardiac hypertrophy is similar to that observed in physiological hypertrophy, which is associated with high cardiac contractility and increased &#945;-myosin heavy chain (&#945;-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 &#946;-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&#8242;,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, &#946;-MHC mRNA expression, PKC activity, and PKC&#949; expression and inhibited &#945;-MHC mRNA expression in cardiomyocytes. T 3 treatment prevented Ang II-induced increases in PKC activity, PKC&#949;, and &#946;-MHC mRNA overexpression and favored &#945;-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. &#169; 2006 NRC Canada.</description.abstract>
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Author Affiliations
  1. Wuhan University
  2. The University of British Columbia