Key result
Overexpression of striatin increased the spontaneous contraction rate of cultured cardiomyocytes by approximately 2-fold, while its knockdown reduced the contraction rate by about 40%.
Why the study?
Does adenoviral-mediated overexpression or knockdown of striatin alter the spontaneous contraction rate in cultured rat ventricular cardiomyocytes?
Does adenoviral-mediated overexpression or knockdown of striatin alter the spontaneous contraction rate in cultured rat ventricular cardiomyocytes?
Striatin regulates the spontaneous contraction rate of ventricular cardiomyocytes and modulates the stability of the Cav-3/CaM complex, suggesting a novel role in cardiac excitation-contraction coupling.
No immediate clinical role; leaves open striatin as a target for cardiac contraction research.
Impaired cardiomyocyte contraction rate is detrimental to cardiac function and often lethal. Despite advancements in the field, there is a paucity of information regarding the coordination of molecules implicated in regulating the heart rate. Striatin (STRN) is a dynamic protein with binding domains to calmodulin (CaM) and caveolin (Cav), both of which are regulators of myocardial function. However, its role in cardiomyocyte contraction is not yet determined. Herein, we show that STRN is expressed in cardiomyocytes and is more abundant in atrial myocardium than in ventricles. Cardiac expression of STRN (protein and mRNA) was developmentally regulated with the highest expression being at neonatal stage (day one) and the lowest in adult rats (13 weeks). CaM pulldown assay indicated that the interaction of cardiac STRN with CaM and caveolin-3 (Cav-3) was calcium sensitive. Interestingly, the overexpression of STRN induced an increase (∼2-fold) in the rate of the spontaneous contraction of cultured cardiomyocytes, while the knockdown of STRN reduced their contraction rate (∼40%). The expression level of STRN was inversely proportional to the interaction of Cav-3 with the CaM/STRN complex. Collectively, our data delineate a novel role for STRN in regulating cardiomyocyte spontaneous contraction rate and the dynamics of the STRN/Cav-3/CaM complex.
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Nader et al. (2017) studied this question. Striatin overexpression or knockdown vs. Control (RFP alone or scrambled shRNA) was evaluated on Spontaneous contraction rate of cultured cardiomyocytes. Overexpression of striatin increased the spontaneous contraction rate of cultured cardiomyocytes by approximately 2-fold, while its knockdown reduced the contraction rate by about 40%.
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