Universidad Complutense de Madrid
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Epidermal Growth Factor Impairs Palatal Shelf Adhesion and Fusion in the T gf-β3 Null Mutant

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Barrio Asensio, María del Carmen y Río Sevilla, Aurora, del y Murillo González, Jorge Alfonso y Maldonado Bautista, Estela y López Gordillo, Yamila y Paradas Lara, Irene y Hernandes, Luzmarina y Catón Vázquez, Javier y Martínez Álvarez, Concepción (2014) Epidermal Growth Factor Impairs Palatal Shelf Adhesion and Fusion in the T gf-β3 Null Mutant. Cells Tissues Organs, 199 (2-3). pp. 201-2011. ISSN 1422-6405

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URL Oficial: http://dx.doi.org/10.1159/000362227




Resumen

The cleft palate presented by transforming growth factor-β3 (Tgf-β3 ) null mutant mice is caused by altered palatal shelf adhesion, cell proliferation, epithelial-to-mesenchymal transformation and cell death. The expression of epidermal growth factor (EGF), transforming growth factor-β1 ( Tgf-β1 ) and muscle segment homeobox-1 (Msx-1) is modified in the palates of these knockout mice, and the cell proliferation defect is caused by the change in EGF expression. In this study, we aimed to determine whether this change in EGF expression has any effect on the other mechanisms altered in Tgf-β 3 knockout mouse palates. We tested the effect of inhibiting
EGF activity in vitro in the knockout palates via the addition of Tyrphostin AG 1478. We also investigated possible interactions between EGF, Tgf-β 1 and Msx-1 in Tgf-β 3 null mouse palate cultures. The results show that the inhibition of EGF activity in Tgf-β 3 null mouse palate cultures improves palatal shelf adhesion and fusion, with a particular effect on cell death, and restores the normal distribution pattern of Msx-1 in the palatal esenchyme. Inhibition of TGF-β 1 does not affect either EGF or Msx-1 expression.


Tipo de documento:Artículo
Información Adicional:

Accepted after revision: March 14, 2014
Published online: May 23, 2014

Palabras clave:Tgf-beta3 ; Tgf-beta1 ; Epidermal growth factor; Msx-1; Knockout; Palate development
Materias:Ciencias Biomédicas > Medicina
Ciencias Biomédicas > Medicina > Fisiología
Ciencias Biomédicas > Medicina > Neurociencias
Ciencias Biomédicas > Medicina > Odontología
Código ID:38561
Depositado:07 Sep 2016 12:58
Última Modificación:19 Sep 2016 10:31

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