Premium
Tenascin‐C in developing mouse teeth: expression of splice variants and stimulation by TGFβ and FGF
Author(s) -
Sahlberg Carin,
Aukhil Ikramuddin,
Thesleff Irma
Publication year - 2001
Publication title -
european journal of oral sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.802
H-Index - 93
eISSN - 1600-0722
pISSN - 0909-8836
DOI - 10.1034/j.1600-0722.2001.00990.x
Subject(s) - mesenchyme , tenascin , dental papilla , tenascin c , fibroblast growth factor , microbiology and biotechnology , biology , in situ hybridization , odontoblast , fibronectin , extracellular matrix , messenger rna , mesenchymal stem cell , pathology , genetics , gene , pulp (tooth) , receptor , medicine
Tenascin‐C is a protein of the extracellular matrix which has been suggested to regulate organogenesis. We have analysed the expression of tenascin‐C mRNA during mouse tooth development. We show that it is transiently expressed during epithelial budding in the condensed dental mesenchyme, and that it reappears later in the dental papilla mesenchyme where it persists in the dental pulp but is downregulated in odontoblasts. Probes corresponding to the domains A4, B, and D of the differentially spliced and domain 7 of the constant region of the FNIII‐like domain show similar patterns of hybridization. Dental epithelium has been shown to induce tenascin‐C in early dental mesenchyme, and we show that growth factors in the transforming growth factor β (TGFβ) and fibroblast growth factor (FGF) families can mimic this effect. FGF‐4, ‐8 and TGFβ‐1 proteins were applied locally by beads on dissected dental mesenchyme, and tenascin‐C expression was analysed after 24 h culture by reverse transcriptase‐polymerase chain reaction (RT‐PCR) in situ hybridization, and immunohistochemistry. FGF‐4 and TGFβ‐1 stimulated tenascin‐C expression in E12 dental mesenchymes. RT‐PCR showed induction of several tenascin‐C isoforms by both TGFβ‐1 and FGFs. We conclude that several splice forms are expressed during mouse tooth development, and that TGFβ‐ and FGF‐family growth factors may act as epithelial signals inducing tenascin expression in the dental mesenchyme.