Thyroid hormone modulates CaMKII δ levels in cultured neonatal cardiomyocytes (LB48)

Previous studies have implicated that intracellular calcium ion (Ca2+) is a mediator in the regulation of cardiac remodeling. Changes in intracellular Ca2+ concentration regulate the activity of several kinases, including Ca2+/calmodulin dependent kinase II δ (CaMKII δ), the predominant cardiac form involved to hypertrophy. Disorders in Ca2+ homeostasis, cardiac hypertrophy and contractile dysfunction are important features observed in hyperthyroidism, however, the contribution of CaMKII δ in cardiomyocyte growth mediated by thyroid hormones (TH) was not been elucidated yet. In the present study, we evaluated the non‐genomic and genomic effects of TH on CaMKII δ levels in neonatal rat cardiomyocytes. Cardiomyocyte primary cultures (n=3) were obtained from 1‐ to 3‐day‐old Wistar rat by enzymatic disaggregation. At 72 h after platting, the ventricular cardiomyocytes were treated for 5 min, 10 min, 15 min, 30 min or 24 h, with serum‐free medium (control cells) or serum‐free medium containing T3 (triiodothyronine, 10ηM, Sigma Aldrich). CaMKII δ expression of was evaluated by Western blot and normalized to GAPDH expression. Data were analyzed by two‐way ANOVA. We found that T3 induced a significant increase (2 fold) on CaMKII δ expression levels only after 24 h of treatment (p蠄0.05 vs. control), but no effect was observed after rapid treatment with T3. The involvement of this kinase on cardiac hypertrophy induced by TH will be evaluated lately. Grant Funding Source : Supported by the Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) and the Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)