Document Detail


Time-dependent changes in the expression of thyroid hormone receptor alpha 1 in the myocardium after acute myocardial infarction: possible implications in cardiac remodelling.
MedLine Citation:
PMID:  17389455     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The present study investigated whether changes in thyroid hormone (TH) signalling can occur after acute myocardial infarction (AMI) with possible physiological consequences on myocardial performance. TH may regulate several genes encoding important structural and regulatory proteins particularly through the TR alpha 1 receptor which is predominant in the myocardium. AMI was induced in rats by ligating the left coronary artery while sham-operated animals served as controls. This resulted in impaired cardiac function in AMI animals after 2 and 13 weeks accompanied by a shift in myosin isoforms expression towards a fetal phenotype in the non-infarcted area. Cardiac hypertrophy was evident in AMI hearts after 13 weeks but not at 2 weeks. This response was associated with a differential pattern of TH changes at 2 and 13 weeks; T(3) and T(4) levels in plasma were not changed at 2 weeks but T(3) was significantly lower and T(4) remained unchanged at 13 weeks. A twofold increase in TR alpha 1 expression was observed after 13 weeks in the non-infarcted area, P<0.05 versus sham operated, while TR alpha 1 expression remained unchanged at 2 weeks. A 2.2-fold decrease in TR beta 1 expression was found in the non-infarcted area at 13 weeks, P<0.05, while no change in TR beta 1 expression was seen at 2 weeks. Parallel studies with neonatal cardiomyocytes showed that phenylephrine (PE) administration resulted in 4.5-fold increase in the expression of TR alpha 1 and 1.6-fold decrease in TR beta 1 expression versus untreated, P<0.05. In conclusion, cardiac dysfunction which occurs at late stages after AMI is associated with increased expression of TR alpha 1 receptor and lower circulating tri-iodothyronine levels. Thus, apo-TR alpha 1 receptor state may prevail contributing to cardiac fetal phenotype. Furthermore, down-regulation of TR beta 1 also contributes to fetal phenotypic changes. alpha1-adrenergic signalling is, at least in part, involved in this response.
Authors:
Constantinos Pantos; Iordanis Mourouzis; Christodoulos Xinaris; Alexandros D Kokkinos; Konstantinos Markakis; Antonios Dimopoulos; Matthew Panagiotou; Theodosios Saranteas; Georgia Kostopanagiotou; Dennis V Cokkinos
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Publication Detail:
Type:  In Vitro; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  European journal of endocrinology / European Federation of Endocrine Societies     Volume:  156     ISSN:  0804-4643     ISO Abbreviation:  Eur. J. Endocrinol.     Publication Date:  2007 Apr 
Date Detail:
Created Date:  2007-03-28     Completed Date:  2007-06-06     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9423848     Medline TA:  Eur J Endocrinol     Country:  England    
Other Details:
Languages:  eng     Pagination:  415-24     Citation Subset:  IM    
Affiliation:
Department of Pharmacology, University of Athens, 75 Mikras Asias Avenue, 11527 Goudi, Athens, Greece. cpantos@cc.uoa.gr
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MeSH Terms
Descriptor/Qualifier:
Animals
Cardiomegaly / etiology
Cardiotonic Agents / pharmacology
Cell Shape
Echocardiography
Isometric Contraction
Male
Myocardial Contraction
Myocardial Infarction / complications,  metabolism*,  physiopathology
Myocardium / metabolism*,  pathology
Myocytes, Cardiac / drug effects,  metabolism,  pathology
Phenylephrine
Rats
Rats, Wistar
Thyroid Hormone Receptors alpha / metabolism*
Thyroid Hormone Receptors beta / metabolism
Thyroxine / metabolism
Time Factors
Triiodothyronine / metabolism
Ventricular Remodeling
Chemical
Reg. No./Substance:
0/Cardiotonic Agents; 0/Thyroid Hormone Receptors alpha; 0/Thyroid Hormone Receptors beta; 59-42-7/Phenylephrine; 6893-02-3/Triiodothyronine; 7488-70-2/Thyroxine

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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