Abstract
Cardiac cells generate and amplify force in the context of cardiac load, yet the membranous sheath enclosing the fibers, the sarcolemma, does not experience displacement. The fact that the sarcolemma sustains beat-to-beat pressure changes without experiencing significant distortion is the muscle contraction paradox the authors sought to resolve. 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 for the nonlinear properties of contraction. The functional significance of prestin is underpinned by alterations of cardiac contractility in Prestin knockout mice. Prestin was previously considered exclusive to outer hair cells of the inner ear; however, our results show that prestin serves a broader cellular motor function.
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