Key result
Loss of Caveolin-1 in adult zebrafish led to significantly decreased ejection fraction and heart rate, increased cardiac cell stiffness, and a transient decrease in cardiomyocyte proliferation.
Why the study?
Caveolin-1 is the primary structural protein of caveolae involved in mechanoprotection, but the impact of its loss on adult heart function and response to cryoinjury was unknown.
Loss of Caveolin-1 in zebrafish leads to increased cardiac cell stiffness and impaired cardiac function, but does not prevent heart regeneration after cryoinjury.
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Zebrafish cav1-KO impairs cardiac function; leaves open caveolae relevance to human injury response.
Caveolin-1 is the main structural protein of caveolae, small membrane invaginations involved in signal transduction and mechanoprotection. Here, we generated cav1-KO zebrafish lacking Cav1 and caveolae, and investigated the impact of this loss on adult heart function and response to cryoinjury. We found that cardiac function was impaired in adult cav1-KO fish, which showed a significantly decreased ejection fraction and heart rate. Using atomic force microscopy, we detected an increase in the stiffness of epicardial cells and cortical myocardium lacking Cav1/caveolae. This loss of cardiac elasticity might explain the decreased cardiac contraction and function. Surprisingly, cav1-KO mutants were able to regenerate their heart after a cryoinjury but showed a transient decrease in cardiomyocyte proliferation.
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Grivas et al. (2020) studied Cardiac function and regeneration. Loss of Caveolin-1 and caveolae (cav1-KO) vs. Wild-type/control zebrafish was evaluated on Cardiac function (ejection fraction and heart rate), cell stiffness, and response to cryoinjury. Loss of Caveolin-1 in adult zebrafish led to significantly decreased ejection fraction and heart rate, increased cardiac cell stiffness, and a transient decrease in cardiomyocyte proliferation.
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