ArticleDifferentiation; research in biological diversity2008
Alteration of medial-edge epithelium cell adhesion in two Tgf-beta3 null mouse strains.
Article in Differentiation; research in biological diversity, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 33 citations in OpenAlex.
- Transforming growth factor β3 deficiency promotes defective lipid metabolism and fibrosis in murine kidney.Disease models & mechanisms · 2021Article
- Extracellular Matrix Remodeling During Palate Development.Organogenesis · 2020Review
- Maternal folic acid supplementation reduces the severity of cleft palate in Tgf-βPediatric research · 2019Article
- Alteration of lens and retina textures from mice embryos with folic acid deficiency: image processing analysis.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2019Article
- TGF-β Signaling and the Epithelial-Mesenchymal Transition during Palatal Fusion.International journal of molecular sciences · 2018Review
- Development of an organotypic stem cell model for the study of human embryonic palatal fusion.Birth defects research · 2018Article
- Article
- Intra-amniotic transient transduction of the periderm with a viral vector encoding TGFβ3 prevents cleft palate in Tgfβ3(-/-) mouse embryos.Molecular therapy : the journal of the American Society of Gene Therapy · 2013Article
- Article
- Putative functions of extracellular matrix glycoproteins in secondary palate morphogenesis.Frontiers in physiology · 2012Article
- The mechanism of TGF-β signaling during palate development.Oral diseases · 2011Review
- Palate morphogenesis: current understanding and future directions.Birth defects research. Part C, Embryo today : reviews · 2010Review
- Tbx22null mice have a submucous cleft palate due to reduced palatal bone formation and also display ankyloglossia and choanal atresia phenotypes.Human molecular genetics · 2009Article
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Authors and funding
14 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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-beta3 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-beta3 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 alpha5- and beta1-integrins, and ICAM-1; in situ hybridization with a Nectin-1 riboprobe; and palatal shelf cultures treated or untreated with TGF-beta3 or neutralizing antibodies against fibronectin or the alpha5-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-beta3 null mutants; the importance of TGF-beta3 to restore their normal pattern of expression; and the crucial role of fibronectin and the alpha5-integrin in palatal shelf adhesion. We thus provide insight into the molecular bases of this important process and the cleft palate presented by Tgf-beta3 null mutant mice.
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