Expression of KLF5 in odontoblastic differentiation of dental pulp cells during <i>in vitro</i> odontoblastic induction and <i>in vivo</i> dental repair

Han, Ning; Chen, Z.; Zhang, Q.

doi:10.1111/iej.12672

Cited by 13 publications

(17 citation statements)

References 25 publications

(57 reference statements)

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“…Specifically, Liu et al [] performed miRNA‐profiling assays of mouse odontoblast differentiation and revealed that the knockdown of miR‐143 promoted odontoblast differentiation both in vivo and in vitro. Several studies revealed that ALP activity was significantly decreased during odontoblastic differentiation [Kim et al, ; Han et al, ; Woo et al, ]. Furthermore, the suppression of DPSC odontoblast differentiation also led to fewer mineralized nodules [Rao et al, ].…”

Section: Discussionmentioning

confidence: 99%

Retracted: The Role of MicroRNA‐143‐5p in the Differentiation of Dental Pulp Stem Cells into Odontoblasts by Targeting Runx2 via the OPG/RANKL Signaling Pathway

Zhan

Liu

Wang

2017

J of Cellular Biochemistry

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This study aims to elucidate the mechanisms by which microRNA-143-5p (miR-143-5p) targets runt-related transcription factor 2 (Runx2) in the differentiation of dental pulp stem cells (DPSCs) into odontoblasts, through regulating the osteoprotegerin receptor activator of the nuclear factor-kB ligand (OPG/RANKL) signaling pathway. Following transfection, DPSCs were divided into blank, control, miR-143-5p mimics, miR-143-5p inhibitors, miR-143-5p inhibitors þ siRunx2 and siRunx2 groups. Alkaline phosphatase (ALP) activity and mineralized nodules were detected using ALP kit and alizarin red staining. Quantitative reverse transcriptase real time PCR (qRT-PCR) was conducted to measure mRNA expressions of miR-143-5p, Runx2, OPG, and RANKL. Western blotting was used to assess protein expression of odontoblast differentiation-related proteins. Transwell assay and an extracellular matrix (ECM) adhesion cell assay were employed to examine cell migration and cell adhesion. Compared with the blank group, the miR-143-5p mimics and siRunx2 groups showed decreased ALP activity, decreased mineralized nodules and displays of calcium. Fewer migrated cells, weakened cell adhesion, decreased protein expression of dentin phosphoprotein (DPP), dentin sialoprotein (DSP), dentin matrix protein 1 (DMP1), osteopontin (OPN), bone sialoprotein (BSP), osteocalcin (OCN), OPG and Runx2, and increased RANKL protein expressions were observed. Additionally, opposite results were observed in the miR-143-5p inhibitors group, demonstrating that down-regulated miR-143-5p promotes the differentiation of DPSCs into odontoblasts by enhancing Runx2 expression via the OPG/RANKL signaling pathway. Based on findings in this study, it is postulated that the enhancement of Runx2 expression via the regulation of the OPG/RANKL signaling pathway could be a beneficial approach for dental pulp regeneration.

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Section: Discussionmentioning

confidence: 99%

Retracted: The Role of MicroRNA‐143‐5p in the Differentiation of Dental Pulp Stem Cells into Odontoblasts by Targeting Runx2 via the OPG/RANKL Signaling Pathway

Zhan

Liu

Wang

2017

J of Cellular Biochemistry

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“…In this study, iMDP-3 cells were grown in differentiation medium, and the mRNA level of Dspp and Dmp1 was upregulated during odontoblastic induction. These results were consistent with our previous observation 25 . Similar to Dspp and Dmp1, Klf5 expression was gradually upregulated in mouse dental papilla mesenchymal cell differentiation and mineralization.…”

Section: Discussionsupporting

confidence: 94%

“…In addition, in reparative dentine formation study, Klf5 was expressed in the odontoblast-like cells and DPCs beneath the perforation sites. These data indicate Klf5 participates in odontoblastic differentiation and reparative dentine formation25. Although Klf5 plays dual biological roles in cell proliferation, differentiation and migration via regulation of its target genes234525, the role of Klf5 in odontoblastic differentiation is still not clear.…”

Section: Discussionmentioning

confidence: 99%

“…Several members of Klf family, including Klf4 24 34 , Klf5 24 25 and Klf10 35 , display distinctive expression patterns in murine tooth development and dental papilla mesenchymal cells (DPCs) as well as are necessary for odontoblastic differentiation of DPCs. Klf4 and Klf5 exhibited specifically spatiotemporal and complementary expression patterns, it suggested that Klf4 and Klf5 may have different roles in differentiation and mineralization of odontoblasts 24 .…”

Section: Discussionmentioning

confidence: 99%

“…Moreover, Klf5-overexpressing transgenic mice affect epidermal development and craniofacial morphogenesis by the arrested molar development at the early bud-stage6. Furthermore, our previous studies demonstrated that Klf5 was highly expressed in the human dental pulp cells and Klf5 knock-down disrupted odontoblastic differentiation25. However, the precise mechanisms of Klf5 in odontoblast differentiation are still unclear.…”

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confidence: 99%

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Klf5 Mediates Odontoblastic Differentiation through Regulating Dentin-Specific Extracellular Matrix Gene Expression during Mouse Tooth Development

Chen

Zhang

Wang³

et al. 2017

Sci Rep

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Klf5, a member of the Krüppel-like transcription factor family, has essential roles during embryonic development, cell proliferation, differentiation, migration and apoptosis. This study was to define molecular mechanism of Klf5 during the odontoblastic differentiation. The expression of Klf5, odontoblast-differentiation markers, Dspp and Dmp1 was co-localized in odontoblastic cells at different stages of mouse tooth development and mouse dental papilla mesenchymal cells. Klf5 was able to promote odontoblastic differentiation and enhance mineral formation of mouse dental papilla mesenchymal cells. Furthermore, overexpression of Klf5 could up-regulate Dspp and Dmp1 gene expressions in mouse dental papilla mesenchymal cells. In silico analysis identified that several putative Klf5 binding sites in the promoter and first intron of Dmp1 and Dspp genes that are homologous across species lines. Electrophoretic mobility shift assay and chromatin immunoprecipitation analysis indicated that Klf5 bound to these motifs in vitro and in intact cells. The responsible regions of Dmp1 gene were located in the promoter region while effect of Klf5 on Dspp activity was in the first intron of Dspp gene. Our results identify Klf5 as an activator of Dmp1 and Dspp gene transcriptions by different mechanisms and demonstrate that Klf5 plays a pivotal role in odontoblast differentiation.

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The histone deacetylase inhibitor, entinostat (MS-275), induces the odontogenic differentiation of an odontoblast-like cell line in the absence of an osteoblast mineralization medium

et al. 2021

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Expression of KLF5 in odontoblastic differentiation of dental pulp cells during in vitro odontoblastic induction and in vivo dental repair

Abstract: KLF5 might be involved in the process of odontoblastic differentiation during reparative dentine formation.

Cited by 13 publications

References 25 publications

Retracted: The Role of MicroRNA‐143‐5p in the Differentiation of Dental Pulp Stem Cells into Odontoblasts by Targeting Runx2 via the OPG/RANKL Signaling Pathway

Retracted: The Role of MicroRNA‐143‐5p in the Differentiation of Dental Pulp Stem Cells into Odontoblasts by Targeting Runx2 via the OPG/RANKL Signaling Pathway

Klf5 Mediates Odontoblastic Differentiation through Regulating Dentin-Specific Extracellular Matrix Gene Expression during Mouse Tooth Development

The histone deacetylase inhibitor, entinostat (MS-275), induces the odontogenic differentiation of an odontoblast-like cell line in the absence of an osteoblast mineralization medium

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