We have located links that may give you full text access.
Journal Article
Research Support, Non-U.S. Gov't
Effects of homeobox gene distal-less 3 on proliferation and odontoblastic differentiation of human dental pulp cells.
Journal of Endodontics 2012 November
INTRODUCTION: Homeodomain gene Distal-less-3 (Dlx3) plays an essential role in tooth development. The aim of this study was to investigate the effects of Dlx3 on proliferation and odontoblastic differentiation of human dental pulp cells (hDPCs).
METHODS: Human DPCs were infected by recombinant lentivirus to overexpress Dlx3 stably, and the biological effects of Dlx3 on the hDPCs were investigated. Proliferation of the hDPCs was measured by direct cell counting and 5-ethynyl-2'-deoxyuridine incorporation assay. Odontogenic differentiation of hDPCs was evaluated by von Kossa staining and alkaline phosphatase activity assay. Important mineral genes such as dentin sialophosphoprotein (DSPP), dentin matrix acidic phosphoprotein 1 (DMP1), alkaline phosphatase (ALP), and nestin (Nes) were determined by real-time polymerase chain reaction. Western blot analysis was performed to determine the difference of expressions of protein of dentin sialophosphoprotein (DSP) and DMP1 with or without the presence of exogenous Dlx3.
RESULTS: Overexpression of Dlx3 decreased the proliferation ability of hDPCs. Dlx3 enhanced differentiation of hDPCs with promoting mineralization nodule formation and up-regulated the ALP activity as well as the expressions of mineralization-related genes including DSPP, DMP1, ALP, and Nes. Meanwhile, the protein levels of DSP and DMP1 significantly increased in the presence of exogenous Dlx3.
CONCLUSIONS: Dlx3 is a potent regulator for proliferation and odontoblastic differentiation of hDPCs.
METHODS: Human DPCs were infected by recombinant lentivirus to overexpress Dlx3 stably, and the biological effects of Dlx3 on the hDPCs were investigated. Proliferation of the hDPCs was measured by direct cell counting and 5-ethynyl-2'-deoxyuridine incorporation assay. Odontogenic differentiation of hDPCs was evaluated by von Kossa staining and alkaline phosphatase activity assay. Important mineral genes such as dentin sialophosphoprotein (DSPP), dentin matrix acidic phosphoprotein 1 (DMP1), alkaline phosphatase (ALP), and nestin (Nes) were determined by real-time polymerase chain reaction. Western blot analysis was performed to determine the difference of expressions of protein of dentin sialophosphoprotein (DSP) and DMP1 with or without the presence of exogenous Dlx3.
RESULTS: Overexpression of Dlx3 decreased the proliferation ability of hDPCs. Dlx3 enhanced differentiation of hDPCs with promoting mineralization nodule formation and up-regulated the ALP activity as well as the expressions of mineralization-related genes including DSPP, DMP1, ALP, and Nes. Meanwhile, the protein levels of DSP and DMP1 significantly increased in the presence of exogenous Dlx3.
CONCLUSIONS: Dlx3 is a potent regulator for proliferation and odontoblastic differentiation of hDPCs.
Full text links
Related Resources
Trending Papers
Challenges in Septic Shock: From New Hemodynamics to Blood Purification Therapies.Journal of Personalized Medicine 2024 Februrary 4
Molecular Targets of Novel Therapeutics for Diabetic Kidney Disease: A New Era of Nephroprotection.International Journal of Molecular Sciences 2024 April 4
The 'Ten Commandments' for the 2023 European Society of Cardiology guidelines for the management of endocarditis.European Heart Journal 2024 April 18
A Guide to the Use of Vasopressors and Inotropes for Patients in Shock.Journal of Intensive Care Medicine 2024 April 14
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app
All material on this website is protected by copyright, Copyright © 1994-2024 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.
By using this service, you agree to our terms of use and privacy policy.
Your Privacy Choices
You can now claim free CME credits for this literature searchClaim now
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app