| Title | DLX3 mutation negatively regulates odontogenic differentiation of human dental pulp cells |
| Authors | Zeng, Li Zhao, Na Han, Dong Liu, Haochen Liu, Yang Wang, Yixiang Feng, Hailan |
| Affiliation | Peking Univ, Sch & Hosp Stomatol, Dept Prosthodont, Beijing, Peoples R China. Peking Univ, Sch & Hosp Stomatol, Cent Lab, Beijing, Peoples R China. Peking Univ, Sch & Hosp Stomatol, Dept Prosthodont, Beijing, Peoples R China. Wang, YX (reprint author), Peking Univ, Sch & Hosp Stomatol, Cent Lab, Beijing, Peoples R China. |
| Keywords | DLX3 mutation Odontogenic differentiation Human dental pulp cells Tricho-dento-osseous syndrome TRICHODENTOOSSEOUS SYNDROME STEM-CELLS EXPRESSION GENE PROLIFERATION AMELOGENESIS HAIR MICE |
| Issue Date | 2017 |
| Publisher | ARCHIVES OF ORAL BIOLOGY |
| Citation | ARCHIVES OF ORAL BIOLOGY.2017,77,12-17. |
| Abstract | Objectives: The purpose of this study was to investigate the role of a novel mutant DLX3 on the odontogenic differentiation of human dental pulp cells (hDPCs) in tricho-dento-osseous (TDO) syndrome. Design: hDPCs were obtained from the healthy premolars, stably-expressing wild-type DLX3 (WT), novel mutant DLX3 (Mu) and control vector (NC) cells were generated using recombinant lentiviruses. The proliferation rates of WT-hDPCs and Mu-hDPCs were measured by CCK8 assay. Odonto-differentiation of hDPCs was assessed by alkaline phosphatase (ALP) activity assay, and mineralization ability was assessed by Alizarin red staining. Odontogenic markers, including DMP-1, DSPP, Nes, ALP, and DLX5, were analyzed using real-time polymerase chain reaction (qPCR). DMP-1 and DSPP expressions were further confirmed by Western blotting. Results: CCK8 results showed that the novel mutant DLX3 decreased the proliferation rate of hDPCs compared with wild-type DLX3. qPCR showed that the novel mutant DLX3 weakened odontogenic differentiation by downregulating the expression of odontogenic genes. These results were further confirmed by Western blotting and ALP activity assay. Additionally, Alizarin red staining showed that the novel mutant DLX3 decreased the mineralization of hDPCs compared with wild-type DLX3. Conclusions: Novel de novo mutation of DLX3 significantly decreases the proliferation rate and inhibits the odontogenic differentiation and mineralization of hDPCs, suggesting that this novel mutation of DLX3 can influence the dentinogenesis in TDO syndrome. (C) 2017 Elsevier Ltd. All rights reserved. |
| URI | http://hdl.handle.net/20.500.11897/473750 |
| ISSN | 0003-9969 |
| DOI | 10.1016/j.archoralbio.2017.01.011 |
| Indexed | SCI(E) |
| Appears in Collections: | 口腔医院 |
