Bone Morphogenetic Protein Receptor Type II Promotes Odontogenic Differentiation of Human Dental Pulp Stem Cells Via Runt-related Transcription Factor 2.

IF 0.9
Jing Lei Zheng, Kai Sun, Bi Chen Lin, Hang Bo Liu, Lan Xin Su, Hao Chen Liu, Hai Lan Feng, Yang Liu, Miao Yu, Dong Han
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Abstract

Objective: To investigate the molecular mechanism by which bone morphogenetic protein receptor type 2 (BMPR2) regulates the odontogenic differentiation of dental pulp stem cells.

Methods: Human dental pulp stem cells (hDPSCs) with lentiviral vector-mediated BMPR2 overexpression and knockdown were generated. Cell proliferation was assessed using a cell counting kit-8 assay. The odontogenic differentiation potential of hDPSCs was examined using alkaline phosphatase and alizarin red S staining. The expression of odontogenic differentiation markers and critical mediators of bone morphogenetic protein (BMP)-suppressor of mothers against decapentaplegic (SMAD) signalling was analysed using real-time quantitative polymerase chain reaction and western blotting.

Results: BMPR2 overexpression promoted odontogenic differentiation of hDPSCs but suppressed their proliferation, which was contrary to the findings in the BMPR2 knockdown group. Moreover, BMPR2 overexpression activated the BMP-SMAD-Runt-related transcription factor 2 (RUNX2) signalling cascade. RUNX2 overexpression partially recaptured the effects of BMPR2 knockdown on odontogenic differentiation of hDPSCs.

Conclusion: These results indicate that BMPR2 promotes odontogenic differentiation of hDPSCs by activating BMPR2-SMAD1/5/8-RUNX2 signalling, and that targeting this cascade could be a promising strategy for gene therapy in human tooth development.

骨形态发生蛋白受体II型通过矮子相关转录因子2促进人牙髓干细胞成牙分化。
目的:探讨骨形态发生蛋白受体2 (BMPR2)调控牙髓干细胞成牙分化的分子机制。方法:制备慢病毒载体介导BMPR2过表达和低表达的人牙髓干细胞(hDPSCs)。使用细胞计数试剂盒-8测定法评估细胞增殖。采用碱性磷酸酶和茜素红S染色检测hdpsc的成牙分化潜能。采用实时定量聚合酶链反应和western blotting分析母鼠抗十肢截瘫(SMAD)信号的成牙分化标志物和骨形态发生蛋白(BMP)抑制因子的表达。结果:BMPR2过表达促进了hDPSCs的成牙性分化,但抑制了其增殖,这与BMPR2敲低组的结果相反。此外,BMPR2过表达激活了bmp - smad - runt相关转录因子2 (RUNX2)信号级联。RUNX2过表达部分重现了BMPR2敲低对hdpsc成牙分化的影响。结论:BMPR2通过激活BMPR2- smad1 /5/8- runx2信号通路促进hDPSCs向牙源性分化,靶向BMPR2- smad1 /5/8- runx2信号通路可能是一种很有前景的人类牙齿发育基因治疗策略。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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