Thyroxine increases Serca2 and Ryr2 gene expression in heart failure rats with euthyroid sick syndrome

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Fábio V. G. Campanha ; Denise Perone ; Dijon H. S. de Campos ; Renata de A. M. Luvizotto ; Maria T. De Síbio ; Miriane de Oliveira ; Regiane M. C. Olimpio ; Fernanda C. F. Moretto ; Carlos R. Padovani ; Gláucia M. F. S. Mazeto ; Antonio C. Cicogna ; Célia R. Nogueira

• Document type: Journal article
• Source: ARCHIVES OF ENDOCRINOLOGY METABOLISM; n. ahead, p. 0-0, 2016.

Abstract

ABSTRACT Objective The current study was aimed at analyzing sarcoplasmic reticulum Ca2+ ATPase (Serca2) and ryanodine receptor type 2 (Ryr2) gene expression in rats subjected to surgery that induced HF and were subsequently treated with T4 using physiological doses. Materials and methods HF was induced in 18 male Wistar rats by clipping the ascending thoracic aorta to generate aortic stenosis (HFS group), while the control group (9-sham) underwent thoracotomy. After 21 weeks, the HFS group was subdivided into two subgroups. One group (9 Wistar rats) with HF received 1.0 µg of T4/100 g of body weight for five consecutive days (HFS/T4); the other group (9 Wistar rats) received isotonic saline solution (HFS/S). The animals were sacrificed after this treatment and examined for signs of HF. Samples from the left ventricles of these animals were analyzed by RT-qPCR for the expression of Serca2 and Ryr2 genes. Results Rats with HF developed euthyroid sick syndrome (ESS) and treatment with T4 restored the T3 values to the Sham level and increased Serca2 and Ryr2 gene expression, thereby demonstrating a possible benefit of T4 treatment for heart function in ESS associated with HF. Conclusion The T4 treatment can potentially normalize the levels of T3 as well elevated Serca2 and Ryr2 gene expression in the myocardium in heart failure rats with euthyroid sick syndrome. (AU)