File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

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

TitleEffects of triiodo-thyronine on angiotensin-induced cardiomyocyte hypertrophy: Reversal of increased β-myosin heavy chain gene expression
Authors
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
Citation
Canadian Journal Of Physiology And Pharmacology, 2006, v. 84 n. 8-9, p. 935-941 How to Cite?
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.
Persistent Identifierhttp://hdl.handle.net/10722/147239
ISSN
2014 Impact Factor: 1.770
2014 SCImago Journal Rankings: 0.611
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorWang, Ben_US
dc.contributor.authorOuyang, Jen_US
dc.contributor.authorXia, Zen_US
dc.date.accessioned2012-05-29T06:00:58Z-
dc.date.available2012-05-29T06:00:58Z-
dc.date.issued2006en_US
dc.identifier.citationCanadian Journal Of Physiology And Pharmacology, 2006, v. 84 n. 8-9, p. 935-941en_US
dc.identifier.issn0008-4212en_US
dc.identifier.urihttp://hdl.handle.net/10722/147239-
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.en_US
dc.languageengen_US
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?cjppen_US
dc.relation.ispartofCanadian Journal of Physiology and Pharmacologyen_US
dc.subject.meshAngiotensinsen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAnimals, Newbornen_US
dc.subject.meshCells, Cultureden_US
dc.subject.meshGene Expression Regulation - Drug Effectsen_US
dc.subject.meshHypertrophy - Chemically Induced - Prevention & Controlen_US
dc.subject.meshLeucine - Metabolismen_US
dc.subject.meshMyocytes, Cardiac - Drug Effects - Metabolism - Pathologyen_US
dc.subject.meshMyosin Heavy Chains - Genetics - Metabolismen_US
dc.subject.meshProtein Isoforms - Genetics - Metabolismen_US
dc.subject.meshProtein Kinase C - Metabolismen_US
dc.subject.meshRna, Messenger - Metabolismen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Wistaren_US
dc.subject.meshThymine - Metabolismen_US
dc.subject.meshTriiodothyronine - Pharmacologyen_US
dc.titleEffects of triiodo-thyronine on angiotensin-induced cardiomyocyte hypertrophy: Reversal of increased β-myosin heavy chain gene expressionen_US
dc.typeArticleen_US
dc.identifier.emailXia, Z:zyxia@hkucc.hku.hken_US
dc.identifier.authorityXia, Z=rp00532en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1139/Y06-043en_US
dc.identifier.pmid17111039en_US
dc.identifier.scopuseid_2-s2.0-33846447480en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33846447480&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume84en_US
dc.identifier.issue8-9en_US
dc.identifier.spage935en_US
dc.identifier.epage941en_US
dc.identifier.isiWOS:000242210800015-
dc.publisher.placeCanadaen_US

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats