miRNAs EN LA REGULACIÓN DE LA DIFERENCIACIÓN DE LAS CÉLULAS DERIVADAS DE EPICARDIO
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2022-07-11
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Jaén: Universidad de Jaén
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[ES] La capa más externa del corazón está constituida por un epitelio denominado epicardio. Durante
el desarrollo cardíaco, las células epicárdicas sufren un proceso de transición epitelio mesénquima
(EMT) (E12.5-E15.5 en ratón). Estas células derivadas de epicardio (EPDCs) migran a través de
la pared miocárdica para terminar constituyendo células endoteliales y fibroblastos, entre otras
poblaciones celulares. Como cabe sospechar, este proceso de EMT al que se enfrentan las células
del epicardio es crucial para un normal desarrollo del corazón en formación. La EMT epicárdica ha
sido ampliamente estudiada en modelos in vitro 3D, identificándose numerosas moléculas con un
papel relevante en este proceso. Entre ellas, el miR-200b podría ser un importante modulador de
la actividad migratoria de las células epicárdicas y EPDCs durante la EMT (datos obtenidos en
nuestro laboratorio aún no publicados). Sin embargo, desconocemos aún si el miR-200b puede
estar modulando el destino celular de las EPDCs que sufren la EMT. Para tratar de averiguarlo,
en este TFG se pretende llevar a cabo un análisis de marcadores típicos endoteliales (ERG),
miocárdicos (mf20) y de fibroblastos (FGFR1 y aSMA), en corazones embrionarios de ratón
(E12.5) en los cuales se ha bloqueado la expresión de miR200b (ensayos de transfección por
pérdida de función) y en corazones en las que este microARN se ha sobreexpresado (ensayos de
transfección por ganancia de función).
[EN] The outermost layer of the heart is made up of an epithelium called the epicardium. During cardiac development, epicardial cells undergo an epithelial-mesenchymal transition (EMT) process (E12.5- E15.5 in mice). These epicardium-derived cells (EPDCs) migrate through the myocardial wall to end up constituting endothelial cells and fibroblasts, among other cell populations. As might be suspected, this EMT process of the epicardium is crucial for the normal development of the developing heart. Epicardial EMT has been extensively studied in vitro 3D models, identifying numerous molecules with a relevant role in this process. Among them, miR-200b could be an important modulator of the migratory activity of epicardial cells and EPDCs during EMT (data obtained in our laboratory not yet published). However, we still do not know if miR-200b may be modulating the cell fate of EPDCs suffering from EMT. To try to find out, in this Degree project we had carried out an analysis of a common endothelial (ERG), myocardial (mf20) and fibroblast (FGFR1 and aSMA) markers, in mouse embryonic hearts (E12.5) in which has blocked the expression of miR200b (loss-of-function transfection assays) and in hearts in which this microRNA has been overexpressed (gain-of-function transfection assays).
[EN] The outermost layer of the heart is made up of an epithelium called the epicardium. During cardiac development, epicardial cells undergo an epithelial-mesenchymal transition (EMT) process (E12.5- E15.5 in mice). These epicardium-derived cells (EPDCs) migrate through the myocardial wall to end up constituting endothelial cells and fibroblasts, among other cell populations. As might be suspected, this EMT process of the epicardium is crucial for the normal development of the developing heart. Epicardial EMT has been extensively studied in vitro 3D models, identifying numerous molecules with a relevant role in this process. Among them, miR-200b could be an important modulator of the migratory activity of epicardial cells and EPDCs during EMT (data obtained in our laboratory not yet published). However, we still do not know if miR-200b may be modulating the cell fate of EPDCs suffering from EMT. To try to find out, in this Degree project we had carried out an analysis of a common endothelial (ERG), myocardial (mf20) and fibroblast (FGFR1 and aSMA) markers, in mouse embryonic hearts (E12.5) in which has blocked the expression of miR200b (loss-of-function transfection assays) and in hearts in which this microRNA has been overexpressed (gain-of-function transfection assays).