Person: Maldonado Bautista, Estela
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First Name
Estela
Last Name
Maldonado Bautista
Affiliation
Universidad Complutense de Madrid
Faculty / Institute
Medicina
Department
Anatomía y Embriología
Area
Anatomía y Embriología Humana
Identifiers
1 results
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Item 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 ConcepciónAlthough 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.