Person: Martín Puig, Silvia
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Item Embryonic echocardiography for assessment of congenital and functional cardiac defects.(STAR Protocols, 2021) Menéndez Montes, Iván; Villalba Orero, María; Escobar, Beatriz; Martín Puig, SilviaCardiac function and morphology by mouse fetal echocardiography can be assessed by scanning the uterus extracted from the abdominal cavity (trans-uterine ultrasound) or the womb (trans-abdominal ultrasound). Advantages of transabdominal ultrasound include (1) non-invasive longitudinal analysis at different stages, reducing animal use; and (2) maintenance of natural environment, diminishing perturbations on functional parameters, which are more frequent in transuterine conditions. Here we describe both approaches, explaining how to identify congenital cardiac defects and defining the correlation between echocardiography findings and histological analysis.Item Activation of amino acid metabolic program in cardiac HIF1-alpha-deficient mice.(iScience, 2021) Menéndez Montes, Iván; Escobar, Beatriz; Gómez, Manuel J.; Albendea Gómez, Teresa; Palacios, Beatriz; Bonzon Kulichenko, Elena; Izquierdo García, José Luis; Alonso, Ana Vanessa; Ferrarini, Alessia; Jiménez Borreguero, Luis Jesús; Ruiz Cabello, Jesús; Vázquez, Jesús; Martín Puig, SilviaHIF1-alpha expression defines metabolic compartments in the developing heart, promoting glycolytic program in the compact myocardium and mitochondrial enrichment in the trabeculae. Nonetheless, its role in cardiogenesis is debated. To assess the importance of HIF1-alpha during heart development and the influence of glycolysis in ventricular chamber formation, herein we generated conditional knockout models of Hif1a in Nkx2.5 cardiac progenitors and cardiomyocytes. Deletion of Hif1a impairs embryonic glycolysis without influencing cardiomyocyte proliferation and results in increased mitochondrial number and transient activation of amino acid catabolism together with HIF2a and ATF4 upregulation by E12.5. Hif1a mutants display normal fatty acid oxidation program and do not show cardiac dysfunction in the adulthood. Our results demonstrate that cardiac HIF1 signaling and glycolysis are dispensable for mouse heart development and reveal the metabolic flexibility of the embryonic myocardium to consume amino acids, raising the potential use of alternative metabolic substrates as therapeutic interventions during ischemic events.