Highlights d Increases in adipose mass lead to an irreversible increase in adipocyte number d Adipocyte number is linked to the adipose expression of a set of growth factors d Among these, only TGFb3 stimulates adipocyte progenitor proliferation d Tgfb3 +/À mice display adipose hypertrophy and glucose intolerance upon weight gain

Tuberosity grafts had more lamina propria and less submocusa, which may be beneficial for volume augmentation.

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-b 3 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-b 3 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 a 5 -and b 1 -integrins, and ICAM-1; in situ hybridization with a Nectin-1 riboprobe; and palatal shelf cultures treated or untreated with TGF-b 3 or neutralizing antibodies against fibronectin or the a 5 -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-b 3 null mutants; the importance of TGF-b 3 to restore their normal pattern of expression; and the crucial role of fibronectin and the a 5 -integrin in palatal shelf adhesion. We thus provide insight into the molecular bases of this important process and the cleft palate presented by Tgf-b 3 null mutant mice.Key words cleft palate Á Tgf-b 3 Á mouse Á collagen Á laminin Á fibronectin Á a 5 b 1 -integrin Á ICAM-1 Á Nectin-1