AI Article Synopsis
- Cardiac cells are essential for generating and amplifying force during heart contractions, but the surrounding membrane, or sarcolemma, remains stable despite pressure changes, creating a paradox.
- Researchers discovered that an elastic protein called prestin enhances force generation in heart cells, which helps explain the nonlinear response of these cells to electrical signals.
- Prestin was thought to only function in the inner ear, but findings indicate it plays an important role in heart muscle contractions and significantly affects heart function when absent.
Article 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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Source |
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8720583 | PMC |
| http://dx.doi.org/10.1016/j.celrep.2021.109097 | DOI Listing |
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