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Transgenic expression of dentin phosphoprotein (DPP) partially rescued the dentin defects of DSPP-null mice.
PLoS One. 2018; 13(4):e0195854.Plos

Abstract

Mutations in the dentin sialophosphoprotein (DSPP) gene cause dentinogenesis imperfecta. After synthesis, DSPP is proteolytically processed into NH2- and COOH-terminal fragments. The NH2-terminal fragment of DSPP is highly glycosylated but not phosphorylated, whereas the COOH-terminal fragment (named "dentin phosphoprotein" or "DPP") is highly phosphorylated but not glycosylated. These two fragments are believed to perform distinct roles in dentin formation. To analyze the functions of DPP in dentinogenesis, we created "Dspp-/-;DPP Tg mice", which expressed transgenic DPP driven by a Type I collagen promoter but lacked the endogenous Dspp gene. We characterized the dentin of the Dspp-/-;DPP Tg mice using X-ray radiography, histology, scanning electron microscopy, double fluorochrome labeling, immunohistochemistry and in situ hybridization. Micro-computed tomography analyses revealed that at postnatal 6 months, the transgenic expression of DPP increased the dentin thickness of the Dspp-null mice by 97.1% and restored the dentin material density by 29.5%. Histological analyses showed that the Dspp-null mice manifested an abnormal widening of the predentin while the predentin in Dspp-/-;DPP Tg mice was narrower than in the Dspp-null mice. Scanning electron microscopy analyses showed that the dentinal tubules in the Dspp-/-;DPP Tg mice were better organized than in the Dspp-null mice. The double fluorochrome labeling analyses demonstrated that the dentin mineral deposition rate in the Dspp-/-;DPP Tg mice was significantly improved compared to that in the Dspp-null mice. These findings indicate that the transgenic expression of DPP partially rescued the dentin defects of the DSPP-null mice, suggesting that DPP may promote dentin formation and that the coordinated actions between DPP and the NH2-terminal fragment of DSPP may be necessary for dentinogenesis.

Authors+Show Affiliations

Department of Biomedical Sciences, Texas A&M University College of Dentistry, Dallas, TX, United States of America.Department of Stomatology, the 2nd Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.Department of Periodontics, Harbin Medical University School of Stomatology, Harbin, Heilongjiang, China.Department of Biomedical Sciences, Texas A&M University College of Dentistry, Dallas, TX, United States of America.Department of Biomedical Sciences, Texas A&M University College of Dentistry, Dallas, TX, United States of America.Department of Biomedical Sciences, Texas A&M University College of Dentistry, Dallas, TX, United States of America.

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural

Language

eng

PubMed ID

29672573

Citation

Zhang, Hua, et al. "Transgenic Expression of Dentin Phosphoprotein (DPP) Partially Rescued the Dentin Defects of DSPP-null Mice." PloS One, vol. 13, no. 4, 2018, pp. e0195854.
Zhang H, Xie X, Liu P, et al. Transgenic expression of dentin phosphoprotein (DPP) partially rescued the dentin defects of DSPP-null mice. PLoS One. 2018;13(4):e0195854.
Zhang, H., Xie, X., Liu, P., Liang, T., Lu, Y., & Qin, C. (2018). Transgenic expression of dentin phosphoprotein (DPP) partially rescued the dentin defects of DSPP-null mice. PloS One, 13(4), e0195854. https://doi.org/10.1371/journal.pone.0195854
Zhang H, et al. Transgenic Expression of Dentin Phosphoprotein (DPP) Partially Rescued the Dentin Defects of DSPP-null Mice. PLoS One. 2018;13(4):e0195854. PubMed PMID: 29672573.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Transgenic expression of dentin phosphoprotein (DPP) partially rescued the dentin defects of DSPP-null mice. AU - Zhang,Hua, AU - Xie,Xiaohua, AU - Liu,Peihong, AU - Liang,Tian, AU - Lu,Yongbo, AU - Qin,Chunlin, Y1 - 2018/04/19/ PY - 2017/12/14/received PY - 2018/03/31/accepted PY - 2018/4/20/entrez PY - 2018/4/20/pubmed PY - 2018/7/24/medline SP - e0195854 EP - e0195854 JF - PloS one JO - PLoS One VL - 13 IS - 4 N2 - Mutations in the dentin sialophosphoprotein (DSPP) gene cause dentinogenesis imperfecta. After synthesis, DSPP is proteolytically processed into NH2- and COOH-terminal fragments. The NH2-terminal fragment of DSPP is highly glycosylated but not phosphorylated, whereas the COOH-terminal fragment (named "dentin phosphoprotein" or "DPP") is highly phosphorylated but not glycosylated. These two fragments are believed to perform distinct roles in dentin formation. To analyze the functions of DPP in dentinogenesis, we created "Dspp-/-;DPP Tg mice", which expressed transgenic DPP driven by a Type I collagen promoter but lacked the endogenous Dspp gene. We characterized the dentin of the Dspp-/-;DPP Tg mice using X-ray radiography, histology, scanning electron microscopy, double fluorochrome labeling, immunohistochemistry and in situ hybridization. Micro-computed tomography analyses revealed that at postnatal 6 months, the transgenic expression of DPP increased the dentin thickness of the Dspp-null mice by 97.1% and restored the dentin material density by 29.5%. Histological analyses showed that the Dspp-null mice manifested an abnormal widening of the predentin while the predentin in Dspp-/-;DPP Tg mice was narrower than in the Dspp-null mice. Scanning electron microscopy analyses showed that the dentinal tubules in the Dspp-/-;DPP Tg mice were better organized than in the Dspp-null mice. The double fluorochrome labeling analyses demonstrated that the dentin mineral deposition rate in the Dspp-/-;DPP Tg mice was significantly improved compared to that in the Dspp-null mice. These findings indicate that the transgenic expression of DPP partially rescued the dentin defects of the DSPP-null mice, suggesting that DPP may promote dentin formation and that the coordinated actions between DPP and the NH2-terminal fragment of DSPP may be necessary for dentinogenesis. SN - 1932-6203 UR - https://www.unboundmedicine.com/medline/citation/29672573/Transgenic_expression_of_dentin_phosphoprotein__DPP__partially_rescued_the_dentin_defects_of_DSPP_null_mice_ L2 - https://dx.plos.org/10.1371/journal.pone.0195854 DB - PRIME DP - Unbound Medicine ER -