Key result
Germ-line deletion of Gas2l3 in mice resulted in decreased cardiomyocyte proliferation, premature binucleation, and development of cardiomyopathy and heart failure after birth.
GAS2L3 plays a central role in cardiomyocyte proliferation and cytokinesis during development, and its deletion leads to cardiomyopathy and heart failure in mice.
No immediate clinical implications from Gas2l3 mouse model; leaves open relevance to human cardiomyopathy pathogenesis.
Significance Here, we demonstrate that mice lacking GAS2L3, a cytoskeleton-associated protein that interacts with actin filaments and tubulin, develop cardiomyopathy and heart failure after birth. During embryogenesis, cardiomyocytes rapidly divide. In the perinatal and neonatal period, cardiomyocytes withdraw from the cell cycle, binucleate, and the further increase in cardiac mass is achieved by hypertrophy. Germ-line deletion of Gas2l3 results in decreased cardiomyocyte proliferation and in cardiomyocyte hypertrophy. Embryonal cardiomyocytes from Gas2l3 -deficient mice exhibit increased expression of the cell cycle inhibitor p21 and display premature binucleation of cardiomyocytes due to defects in cytokinetic abscission. Together these results suggest that GAS2L3 plays a central role in cardiomyocyte proliferation and cytokinesis during development.
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Stopp et al. (2017) studied Cardiomyopathy and heart failure. Germ-line deletion of Gas2l3 vs. Wild-type mice was evaluated on Cardiomyocyte proliferation and cytokinesis. Germ-line deletion of Gas2l3 in mice resulted in decreased cardiomyocyte proliferation, premature binucleation, and development of cardiomyopathy and heart failure after birth.
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