Abstract
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 cells of the cortical zone 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.
Highlights
Caveolin-1 is the main structural protein of caveolae, small membrane invaginations involved in signal transduction and mechanoprotection
Using atomic force microscopy (AFM)-force spectroscopy measurements[25], we detected a substantial reduction in cardiac elasticity in cav1-KO animals
Epicardial cells and cells of the cortical zone in cav1-KO hearts lacking caveolae are stiffer than wild type (WT) counterparts
Summary
Caveolin-1 is the main structural protein of caveolae, small membrane invaginations involved in signal transduction and mechanoprotection. We generated cav1-KO zebrafish lacking Cav[1] and caveolae, and investigated the impact of this loss on adult heart function and response to cryoinjury. Using atomic force microscopy, we detected an increase in the stiffness of epicardial cells and cells of the cortical zone lacking Cav1/caveolae. This loss of cardiac elasticity might explain the decreased cardiac contraction and function. Cav1-KO mutants were able to regenerate their heart after a cryoinjury but showed a transient decrease in cardiomyocyte proliferation. Resection of the ventricular apex in hearts of cav1a mutant zebrafish leads to regeneration defects 30 days post amputation (dpa), because of decreased cardiomyocyte proliferation and increased fibrosis in the amputation p lain[24]. Cav1-KO hearts showed a severe ventricular dysfunction, underscoring the role of caveolae in the mechanical properties and homeostasis of the heart
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