Characterization of AT-1 cardiomyocytes as a model for studies of T3 effects on cardiac cells.

AT-1 cardiomyocyte derive from atrial tumors in transgenic mice. Earlier studies have indicated a highly differentiated, contracting, cardiac phenotype in primary cultures and the AT-1 cardiomyocyte may thus be an excellent in vitro model in cardiac research. Thyroid hormone (T3) has positive inotropic and chronotropic effects and is clinically known to be relevant in various pathological heart conditions. Thyroid Hormone Receptors (TR) are ligand regulated transcriptional activators who mediate the effects of T3. The aim of this study was to determine whether AT-1 cardiomyocytes express TR. Regular binding competition assays showed a Kd of 370 +/- 105 for 125I-T3 binding to TR. Reverse transcription-PCR in mouse showed that TRalpha1, alpha2, beta1 and beta2 mRNA were expressed in AT-1 cardiomyocytes and mouse myocardium. Western blot with polyclonal rabbit antibodies against human TR revealed the presence of TRalpha1, beta2 and low levels of TRbeta1 while TRalpha2 was not detectable. Generally, for the detected subtypes the intensities of the bands were weaker for AT-1 cardiomyocytes in comparison to mouse heart. We conclude that the AT-1 cardiomyocytes express both protein and mRNA for TR and may provide a useful model for studying T3 effects in cultured cardiac myocytes.