Person:
Maldonado Bautista, Estela

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First Name
Estela
Last Name
Maldonado Bautista
URI
https://hdl.handle.net/20.500.14352/79646
Affiliation
Universidad Complutense de Madrid
Faculty / Institute
Medicina
Department
Anatomía y Embriología
Area
Anatomía y Embriología Humana
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2008 - 20092
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Author: Martínez Álvarez, María Concepción × Subject: 611.081.1 ×

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Now showing 1 - 2 of 2
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    Interactions between TGF-beta1 and TGF-beta3 and their role in medial edge epithelium cell death and palatal fusion in vitro
    (Differentiation, 2009) Murillo Arroyo, Francisco Javier; Maldonado Bautista, Estela; Barrio MC; Río Sevilla, Aurora Del; López, Y; Martínez Sanz, Elena; González, I; Martín Álvaro, María Concepción; Casado Gómez, Inmaculada; Martínez Álvarez, María Concepción
    In recent decades, studies have shown that both TGF-b1 and TGF-b3 play an important role in the induction of medial edge epithelium (MEE) cell death and palatal fusion. Many of these experiments involved the addition or blockage of one of these growth factors in wild-type (WT) mouse palate cultures, where both TGF-b1 and TGF-b3 are present. Few studies have addressed the existence of interactions between TGF-b1 and TGF-b3, which could modify their individual roles in MEE cell death during palatal fusion. We carried out several experiments to test this possibility, and to investigate how this could influence TGF-b1 and TGF-b3 actions on MEE cell death and palatal shelf fusion. We double immunolabelled developing mouse palates with anti-TGF-b1 or anti-TGF-b3 antibodies and TUNEL, added rhTGF-b1 or rhTGF-b3 or blocked the TGF-b1 and TGF-b3 action at different concentrations to WT or Tgf-b3 null mutant palate cultures, performed in situ hybridizations with Tgf-b1 or Tgf-b3 riboprobes, and measured the presence of TUNEL-positive midline epithelial seam (MES) cells and MES disappearance (palatal shelf fusion) in the different in vitro conditions. By combining all these experiments, we demonstrate great interaction between TGF-b1 and TGF-b3 in the developing palate and confirm that TGF-b3 has a more active role in MES cell death than TGF-b1, although both are major inductors of MES disappearance. Finally, the co-localization of TGF-b1, but not TGF-b3, with TUNEL in the MES allows us to suggest a possible role for TGF-b1 in MES apoptotic clearance.
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    Alteration of medial-edge epithelium cell adhesion in two Tgf-beta3 null mouse strains
    (Differentiation, 2008) Martínez Sanz, Elena; Río Sevilla, Aurora Del; Barrio Asensio, María Del Carmen; Maldonado Bautista, Estela; Murillo González, Jorge Alfonso; Garcillán, B; Amorós, M; Fuerte, T; Fernández, A; Trinidad, E; Rabadán, MA; López, Y; Martínez Salmeán, María Luisa; Martínez Álvarez, María Concepción
    Although palatal shelf adhesion is a crucial event during palate development, little work has been carried out to determine which molecules are responsible for this process. Furthermore, whether altered palatal shelf adhesion causes the cleft palate presented by Tgf-b3 null mutant mice has not yet been clarified. Here, we study the presence/distribution of some extracellular matrix and cell adhesion molecules at the time of the contact of palatal shelves in both wild-type and Tgf-b3 null mutant palates of two strains of mice (C57/BL/6J(C57), and MF1) that develop cleft palates of different severity. We have performed immunohistochemistry with antibodies against collagens IV and IX, laminin, fibronectin, the a5- and b1-integrins, and ICAM-1; in situ hybridization with a Nectin-1 riboprobe; and palatal shelf cultures treated or untreated with TGF-b3 or neutralizing antibodies against fibronectin or the a5-integrin. Our results show the location of these molecules in the wild-type mouse medial edge epithelium (MEE) of both strains at the time of the contact of palatal shelves; the heavier (C57) and milder (MF1) alteration of their presence in the Tgf-b3 null mutants; the importance of TGF-b3 to restore their normal pattern of expression; and the crucial role of fibronectin and the a5-integrin in palatal shelf adhesion. We thus provide insight into the molecular bases of this important process and the cleft palate presented by Tgf-b3 null mutant mice.