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Time-dependent changes in the expression of thyroid hormone receptor 1 in the myocardium after acute myocardial infarction: possible implications in cardiac remodelling

Department of Pharmacology, University of Athens, 75 Mikras Asias Avenue, 11527 Goudi, Athens, Greece and ¹ 1st Cardiology Department, Onassis Cardiac Surgery Center, 356 Sygrou Avenue, 176 74 Kallithea, Athens, Greece

(Correspondence should be addressed to C Pantos; Email: cpantos{at}cc.uoa.gr)

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 TR1 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; T₃ and T₄ levels in plasma were not changed at 2 weeks but T₃ was significantly lower and T₄ remained unchanged at 13 weeks. A twofold increase in TR1 expression was observed after 13 weeks in the non-infarcted area, P<0.05 versus sham operated, while TR1 expression remained unchanged at 2 weeks. A 2.2-fold decrease in TRß1 expression was found in the non-infarcted area at 13 weeks, P<0.05, while no change in TRß1 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 TR1 and 1.6-fold decrease in TRß1 expression versus untreated, P<0.05. In conclusion, cardiac dysfunction which occurs at late stages after AMI is associated with increased expression of TR1 receptor and lower circulating tri-iodothyronine levels. Thus, apo-TR1 receptor state may prevail contributing to cardiac fetal phenotype. Furthermore, down-regulation of TRß1 also contributes to fetal phenotypic changes. 1-adrenergic signalling is, at least in part, involved in this response.

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				C. Pantos, A. Dritsas, I. Mourouzis, A. Dimopoulos, G. Karatasakis, G. Athanassopoulos, S. Mavrogeni, A. Manginas, and D. V Cokkinos Thyroid hormone is a critical determinant of myocardial performance in patients with heart failure: potential therapeutic implications Eur. J. Endocrinol., October 1, 2007; 157(4): 515 - 520. [Abstract] [Full Text] [PDF]

				C. Pantos, I. Mourouzis, K. Markakis, A. Dimopoulos, C. Xinaris, A. D. Kokkinos, M. Panagiotou, and D. V. Cokkinos Thyroid hormone attenuates cardiac remodeling and improves hemodynamics early after acute myocardial infarction in rats Eur. J. Cardiothorac. Surg., August 1, 2007; 32(2): 333 - 339. [Abstract] [Full Text] [PDF]