ArticleEuropean journal of histochemistry : EJH2016
Transgenic expression of dentin phosphoprotein inhibits skeletal development.
Article in European journal of histochemistry : EJH, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 11 citations in OpenAlex.
- Calcium phosphate polymer induced liquid precursor improves dentin bonding performance of primary teeth with dentinogenesis imperfecta type II.BMC oral health · 2026Article
- DSP and DPP are dispensable for initiation of dentin and enamel mineralization but critical for circumpulpal dentin mineralization.Scientific reports · 2025Article
- Dentine sialophosphoprotein signal in dentineogenesis and dentine regeneration.European cells & materials · 2021Review
- High-Phosphate Diet Improved the Skeletal Development of Fam20c-Deficient Mice.Cells, tissues, organs · 2019Article
- Histochemistry as a versatile research toolkit in biological research, not only an applied discipline in pathology.European journal of histochemistry : EJH · 2018Article
- Transgenic expression of dentin phosphoprotein (DPP) partially rescued the dentin defects of DSPP-null mice.PloS one · 2018Article
- Histochemistry today: Detection and location of single molecules.European journal of histochemistry : EJH · 2017Article
- Phosphorylation regulates the secondary structure and function of dentin phosphoprotein peptides.Bone · 2017Article
- Is there still room for novelty, in histochemical papers?European journal of histochemistry : EJH · 2016Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Dentin sialophosphoprotein (DSPP) is proteolytically processed into an NH2-terminal fragment called dentin sialoprotein (DSP) and a COOH-terminal fragment known as dentin phosphoprotein (DPP). These two fragments are believed to perform distinct roles in formation of bone and dentin. To investigate the functions of DPP in skeletal development, we generated transgenic mice to overexpress hemagglutinin (HA)-tagged DPP under the control of a 3.6 kb type I collagen (Col1a1) promoter (designated as Col1a1-HA-DPP). The Col1a1-HA-DPP transgenic mice were significantly smaller by weight, had smaller skeletons and shorter long bones than their wild type littermates, as demonstrated by X-ray radiography. They displayed reduced trabecular bone formation and narrower zones of proliferative and hypertrophic chondrocytes in the growth plates of the long bones. Histological analyses showed that the transgenic mice had reduced cell proliferation in the proliferating zone, but lacked obvious defects in the chondrocyte differentiation. In addition, the transgenic mice with a high level of transgene expression developed spontaneous long bone fractures. In conclusion, overexpressing DPP inhibited skeletal development, suggesting that the balanced actions between the NH2- and COOH-terminal fragments of DSPP may be required for normal skeletal development.
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Registered trials
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