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oai:repisalud.isciii.es:20.500.12105/252412024-11-28T15:15:07Zcom_20.500.12105_15322com_20.500.12105_2051col_20.500.12105_16927

00925njm 22002777a 4500 dc Prados, Belén author Gómez-Apiñániz, Paula author Papoutsi, Tania author Luxán, Guillermo author Zaffran, Stephane author Pérez-Pomares, José María author de la Pompa, José Luis author Prados, Belén author Gómez-Apiñániz, Paula author Papoutsi, Tania author Luxán, Guillermo author Zaffran, Stephane author Pérez-Pomares, José María author de la Pompa, José Luis author 2018-03-14 During mammalian heart development, restricted myocardial Bmp2 expression is a key patterning signal for atrioventricular canal specification and the epithelial-mesenchyme transition that gives rise to the valves. Using a mouse transgenic line conditionally expressing Bmp2, we show that widespread Bmp2 expression in the myocardium leads to valve and chamber dysmorphogenesis and embryonic death by E15.5. Transgenic embryos show thickened valves, ventricular septal defect, enlarged trabeculae and dilated ventricles, with an endocardium able to undergo EMT both in vivo and in vitro. Gene profiling and marker analysis indicate that cellular proliferation is increased in transgenic embryos, whereas chamber maturation and patterning are impaired. Similarly, forced Bmp2 expression stimulates proliferation and blocks cardiomyocyte differentiation of embryoid bodies. These data show that widespread myocardial Bmp2 expression directs ectopic valve primordium formation and maintains ventricular myocardium and cardiac progenitors in a primitive, proliferative state, identifying the potential of Bmp2 in the expansion of immature cardiomyocytes. 10.1038/s41419-018-0442-z 2041-4889 Cell death & disease http://hdl.handle.net/10668/12240 29540665 https://hdl.handle.net/20.500.12105/25241 Myocardial Bmp2 gain causes ectopic EMT and promotes cardiomyocyte proliferation and immaturity.