MiR-148a-3p Regulates the Invasion and Odontoblastic Differentiation of Human Dental Pulp Stem Cells via the Wnt1/β-Catenin Pathway

Abstract

Background and Objectives MiR-148a-3p has been reported to regulate the differentiation of marrow stromal cell osteoblast. In this study, whether miR-148a-3p regulated the odontoblastic differentiation of human dental pulp stem cells (hDPSCs) or not was explored. Methods and Results The hDPSCs were isolated and identified via flow cytometry. Targets of miR-148a-3p were identified via bioinformatics and dual-luciferase reporter assay. After the cell was cultured in the odontogenic differentiation medium or infected, cell viability, invasion, and odontoblastic differentiation were detected via MTT, transwell, and Alizarin Red S staining, respectively. The miR-148a-3p, Wnt1, β-catenin, DSPP, DMP-1, RUNX2, OCN, and Smad4 expressions were determined by RT-qPCR and Western blot. The hDPSCs odontoblastic differentiation downregulated the miR-148a-3p expression and upregulated Wnt1 expression. Wnt1 was determined as the target for miR-148a-3p. MiR-148a-3p mimic and siWnt1 suppressed the cell viability, invasion, and odontoblastic differentiation of hDPSCs and inhibited the Wnt1, β-catenin, DSPP, DMP-1, RUNX2, OCN, and Smad4 expressions. In contrast, miR-148a-3p inhibitor and overexpressed Wnt1 promoted the cell viability, invasion, and odontoblastic differentiation of hDPSCs, and upregulated the Wnt1, β-catenin, DSPP, DMP-1, RUNX2, OCN, and Smad4 expressions. Also, miR-148a-3p mimic and inhibitor reversed the effects of Wnt1 overexpression and siWnt1. Conclusions MiR-148a-3p modulated the invasion and odontoblastic differentiation of hDPSCs through the Wnt1/β-catenin pathway.

LncRNA-KCNQ1OT1 Promotes the Odontoblastic Differentiation of Dental Pulp Stem Cells via Regulating miR-153-3p/RUNX2 Axis

“…In this study, during the odontoblastic differentiation of DPSCs, the expression of RUNX2 increased, which is consistent with the research results of other scholars [19]. Studies showed many miRNAs regulated the odontoblastic differentiation via targeting on RUNX2 [10,17,25]. In this study, we used targetscan software to found miR-153-3p have the binding site of RUNX2 3'UTR.…”

“…Odontoblastic differentiation of DPSCs involves many factors such as biological scaffolds, regulatory genes and signal pathways [4,14,22,26,27]. MicroRNAs (miRNAs, miRs) as posttranscriptional inhibitors, recognize and bind to the 3'untranslated region (3'UTR) of the target gene to inhibit the translation of the target gene protein, and have complex regulatory effects on the body's physiological/pathological activities, including the process of odontoblastic differentiation [10][11][12]. Long non-coding RNAs (LncRNAs) as competing endogenous RNAs (ceRNAs) play key role in cell cycle, migration, proliferation, differentiation and apoptosis through sponging miRNAs to regulate miRNA targets.…”

LncKCNQ1OT1 Promotes the Odontoblastic Differentiation of Dental Pulp Stem Cells via Regulating hsa-miR-153-3p/RUNX2 Axis

“…In our study, during the odontoblastic differentiation of DPSCs, the expression of RUNX2 increased, which is consistent with the research results of other scholars [ 31 ]. Studies showed many miRNAs regulated the odontoblastic differentiation via targeting on RUNX2 [ 15 , 32 , 33 ]. In our study, we used targetscan software to find whether hsa-miR-153-3p has the binding site of RUNX2 3′UTR.…”

“…Odontoblastic differentiation of DPSCs involves many factors, such as biological scaffolds, regulatory genes, and signal pathways [ 8 , 9 , 10 , 11 , 12 ]. MicroRNAs (miRNAs, miRs), as post-transcriptional inhibitors, recognize and bind to the 3′ untranslated region (3′UTR) of the target gene to inhibit the translation of the target gene protein and have complex regulatory effects on the body’s physiological/pathological activities, including the process of odontoblastic differentiation [ 13 , 14 , 15 ]. Long noncoding RNAs (LncRNAs), as competing endogenous RNAs (ceRNAs), play a key role in cell cycle, migration, proliferation, differentiation, and apoptosis through sponging miRNAs to regulate miRNA targets [ 16 , 17 ].…”