Abstract
Cardiac cells generate and amplify force in the context of cardiac load, yet the membranous sheath enclosing the muscle fibers—the sarcolemma—does not experience displacement. That the sarcolemma sustains beat-to-beat pressure changes without experiencing significant distortion is a muscle-contraction paradox. Here, we report that an elastic element—the motor protein prestin (Slc26a5)—serves to amplify actin-myosin force generation in mouse and human cardiac myocytes, accounting partly for the nonlinear capacitance of cardiomyocytes. The functional significance of prestin is underpinned by significant alterations of cardiac contractility in Prestin-knockout mice. Prestin was previously considered exclusive to the inner ear’s outer hair cells; however, our results show that prestin serves a broader cellular motor function.
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•Prestin is considered to be expressed exclusively in outer hair cells of the inner ear•The current study shows that prestin is expressed in cardiomyocytes•Prestin serves to amplify actin-myosin force generation in cardiomyocytes•Prestin serves a broader cellular motor function
Zhang et al. show that the motor protein prestin (Slc26a5) is expressed in the heart, serving to amplify actin-myosin force generation in cardiomyocytes. Prestin is considered to be expressed exclusively in outer hair cells of the inner ear. However, this study demonstrates prestin’s broader cellular motor function.