Cardiac AKAP12 Signalosome Overexpression Exacerbates Effects of Induced Heart Failure via Decreased SERCA2 Expression



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Heart failure (HF), defined as an impaired ability of the heart to efficiently pump blood, is a leading cause of death. Calcium levels are strictly regulated by the cell and fluctuations can result in inefficient pumping of the heart. In heart failure, basal calcium levels remain high in between contractions, causing reduced contractility. AKAP12 mice were grouped by sex, level of gene expression, and treatment. Heart failure was induced through chronic stimulation of the β-adrenergic receptors. This was achieved by the insertion of subcutaneous osmotic pumps containing Isoproterenol. Post-surgery data was collected on physical assessments using echocardiogram techniques. After a two-week recovery period, hearts from these mice were harvested. Subsequent measurements on gene expression through the use of RT-qPCR on tissue lysates were performed. It was observed that contractility parameters were reduced in AKAP12 OX mice compared to the wild type (WT) mice following 14 days of subcutaneous isoproterenol administration, in both males and females. Additionally, decreased levels of expression of SERCA2 mRNA in AKAP12 OX mice compared to the WT mice were observed. AKAP12 might be a potential target for modulating cardiac function and designing drugs to ameliorate HF. Specifically, AKAP12 could be implicated in calcium regulation.