Barreto-Chaves Maria Luiza M, Carneiro-Ramos Marcela Sorelli, Cotomacci Guilherme, Júnior Marconi Barbosa Coutinho, Sarkis João José Freitas
Laboratory of Cellular Biology and Functional Anatomy, Department of Anatomy, Biomedical Sciences Institute, University of São Paulo, Av. Prof. Lineu Prestes 2415, Cidade Universitária, São Paulo, SP 05508-900, Brazil.
Mol Cell Endocrinol. 2006 Jun 7;251(1-2):49-55. doi: 10.1016/j.mce.2006.02.010. Epub 2006 Apr 3.
Degradation of adenine nucleotides by myocardial cells occurs, in part, by a cascade of surface-located enzymes converting ATP into adenosine that has important implications for the regulation of the nucleotide/nucleoside ratio modulating the cardiac functions. Thyroid hormones have profound effects on cardiovascular system, as observed in hypo- and hyperthyroidism. Combined biochemical parameters and gene expression analysis approaches were used to investigate the influence of tri-iodothyronine (T3) on ATP and ADP hydrolysis by isolated myocytes. Cultures of cardiomyocytes were submitted to increasing doses of T3 for 24h. Enzymatic activity and expression were evaluated. T3 (0.1 nM) caused an increase in ATP and ADP hydrolysis. Experiments with specific inhibitors suggest the involvement of an NTPDase, which was confirmed by an increase in NTPDase 3 messenger RNA (mRNA) levels. Since T3 promotes an increase in the contractile protein, leading to cardiac hypertrophy, it is tempting to postulate that the increase in ATP hydrolysis and the decrease in the extracellular levels signify an important factor for prevention of excessive contractility.
