Noggin inhibition of mouse dentinogenesis
| Autor: | M. Douglas Benson, Hua Zhang, Priyam Jani, Chunlin Qin |
|---|---|
| Rok vydání: | 2019 |
| Předmět: |
0301 basic medicine
Bone sialoprotein animal structures Dentinogenesis imperfecta Sialoglycoproteins Medicine (miscellaneous) General Biochemistry Genetics and Molecular Biology Article 03 medical and health sciences Mice 0302 clinical medicine Dentin sialophosphoprotein stomatognathic system medicine Dentin Animals General Dentistry Extracellular Matrix Proteins biology Chemistry 030206 dentistry Dentinogenesis medicine.disease Phosphoproteins DMP1 Cell biology stomatognathic diseases 030104 developmental biology Odontoblast medicine.anatomical_structure embryonic structures biology.protein Pulp (tooth) Carrier Proteins |
| Zdroj: | J Oral Biosci |
| ISSN: | 1880-3865 |
| Popis: | Objectives The Bone Morphogenetic Proteins (BMPs) direct tooth development and still express in the adult tooth. We hypothesized that inhibition of BMP function would therefore disrupt dentinogenesis by differentiated odontoblasts. Methods We generated mice overexpressing the BMP-inhibitory protein Noggin in differentiated odontoblasts and osteocytes under control of a Dmp1 promoter-driven cre transgene. We compared the dentin phenotype in these mice with that in WT littermates and in mice with a Smad4 odontoblast/osteocyte knockout mediated by the same cre and therefore lacking all BMP and Tgfβ signaling in the same tissues. Results Three-month-old first molars from both Noggin-expressing and Smad4-deleted mice showed decreased dentin volume with enlarged pulp cavities, and both displayed less organized and mineralized dentinal tubules compared to WT. The Smad4-ablated phenotype was more severe. While dentin sialophosphoprotein (DSPP) and bone sialoprotein (BSP) were decreased in the dentin of both lines, dentin matrix protein 1 (DMP1) was sharply increased in Noggin-expressing teeth. Conclusions The phenotypes we observed in Noggin-overexpressing and Smad4-conditional knockout teeth resemble the phenotype of Dentinogenesis Imperfecta (DGI) type III. Our results show that BMPs regulate post-natal dentinogenesis and that BMP-inhibitory proteins like Noggin play a role in that regulation. The increased severity of the Smad4 phenotype indicates that Tgfβ ligands, in addition to BMPs, play a crucial role in post-developmental dentinogenesis. |
| Databáze: | OpenAIRE |
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