17β-Estradiol induces odontoblastic differentiation via activation of the c-Src/MAPK pathway in human dental pulp cells

The present study is aimed at investigating the effects of the exogenous estrogen 17β-estradiol (E2) on odontoblastic differentiation in human dental pulp cells (HDPCs) immotalized with hTERT gene and their molecular mechanism. Proliferation was detected by BrdU assay, and odontoblast differentiation induction was evaluated by the expression of dentin sialophosphoprotein (DSPP), dentin sialoprotein (DSP) and dentin matrix protein1 (DMP1), and alkaline phosphatase (ALP) activity and mineralization. Estrogen receptor-α (ER-α), c-Src, and mitogen-activated protein kinases (MAPKs) were examined and their inhibitors were used to determine the roles on odontogenic induction. E2 significantly promoted the HDPC proliferation, which was mediated by extracellular signal-related kinase 1/2. E2 upregulated DSPP, DSP, and DMP1 as the odontogenic differentiation markers and enhanced ALP activity and mineralization. E2 increased phosphorylation of ER-α and fulvestrant, an ER downregulator, significantly downregulated DSPP, DMP1, and DSP induced by E2. Moreover, E2 treatment activated c-Src and MAPKs upon odontogenic induction, whereas chemical inhibition of c-Src and MAPKs decreased expression of DSPP, DMP1, and DSP and mineralization augmented by E2. Moreover, fulvestrant reduced E2-induced phosphorylation of c-Src and MAPK and inhibition of c-Src by PP2 attenuated activation of MAPKs during E2-induced odontoblastic differentiation. Taken together, these results indicated that E2 stimulates odontoblastic differentiation of HDPCs via coordinated regulation of ER-α, c-Src, and MAPK signaling pathways, which may play a key role in the regeneration of dentin.

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Effects of high-mobility group box 1 on the proliferation and odontoblastic differentiation of human dental pulp cells

International Endodontic Journal ◽

10.1111/iej.12112 ◽

2013 ◽

Vol 46 (12) ◽

pp. 1153-1163 ◽

Cited By ~ 11

Author(s):

S. C. Qi ◽

C. Cui ◽

Y. H. Yan ◽

G. H. Sun ◽

S. R. Zhu

Keyword(s):

Dental Pulp ◽

High Mobility ◽

High Mobility Group ◽

Dental Pulp Cells ◽

Human Dental Pulp Cells ◽

Odontoblastic Differentiation ◽

Human Dental Pulp ◽

Pulp Cells

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Effects of different aperture-sized type I collagen/silk fibroin scaffolds on the proliferation and differentiation of human dental pulp cells

Regenerative Biomaterials ◽

10.1093/rb/rbab028 ◽

2021 ◽

Vol 8 (4) ◽

Author(s):

Shihui Jiang ◽

Zhaoxia Yu ◽

Lanrui Zhang ◽

Guanhua Wang ◽

Xiaohua Dai ◽

...

Keyword(s):

Silk Fibroin ◽

Dental Pulp ◽

Type I Collagen ◽

Type I ◽

Dental Pulp Cells ◽

Human Dental Pulp Cells ◽

Alp Activity ◽

Proliferation And Differentiation ◽

Human Dental Pulp ◽

Pulp Cells

Abstract This study aimed at evaluate the effects of different aperture-sized type I collagen/silk fibroin (CSF) scaffolds on the proliferation and differentiation of human dental pulp cells (HDPCs). The CSF scaffolds were designed with 3D mapping software Solidworks. Three different aperture-sized scaffolds (CSF1–CSF3) were prepared by low-temperature deposition 3D printing technology. The morphology was observed by scanning electron microscope (SEM) and optical coherence tomography. The porosity, hydrophilicity and mechanical capacity of the scaffold were detected, respectively. HDPCs (third passage, 1 × 105 cells) were seeded into each scaffold and investigated by SEM, CCK-8, alkaline phosphatase (ALP) activity and HE staining. The CSF scaffolds had porous structures with macropores and micropores. The macropore size of CSF1 to CSF3 was 421 ± 27 μm, 579 ± 36 μm and 707 ± 43 μm, respectively. The porosity was 69.8 ± 2.2%, 80.1 ± 2.8% and 86.5 ± 3.3%, respectively. All these scaffolds enhanced the adhesion and proliferation of HDPCs. The ALP activity in the CSF1 group was higher than that in the CSF3 groups (P < 0.01). HE staining showed HDPCs grew in multilayer within the scaffolds. CSF scaffolds significantly improved the adhesion and ALP activity of HDPCs. CSF scaffolds were promising candidates in dentine-pulp complex regeneration.

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Sclerostin promotes human dental pulp cells senescence

PeerJ ◽

10.7717/peerj.5808 ◽

2018 ◽

Vol 6 ◽

pp. e5808 ◽

Cited By ~ 4

Author(s):

Yanjing Ou ◽

Yi Zhou ◽

Shanshan Liang ◽

Yining Wang

Keyword(s):

Dental Pulp ◽

Wnt Signaling Pathway ◽

Dental Pulp Cells ◽

Differentiation Potential ◽

Human Dental Pulp Cells ◽

Qrt Pcr ◽

Odontoblastic Differentiation ◽

Human Dental Pulp ◽

Pulp Cells

Background Senescence-related impairment of proliferation and differentiation limits the use of dental pulp cells for tissue regeneration. Deletion of sclerostin improves the dentinogenesis regeneration, while its role in dental pulp senescence is unclear. We investigated the role of sclerostin in subculture-induced senescence of human dental pulp cells (HDPCs) and in the senescence-related decline of proliferation and odontoblastic differentiation. Methods Immunohistochemical staining and qRT-PCR analyses were performed to examine the expression pattern of sclerostin in young (20–30-year-old) and senescent (45–80-year-old) dental pulps. HDPCs were serially subcultured until senescence, and the expression of sclerostin was examined by qRT-PCR analysis. HDPCs with sclerostin overexpression and knockdown were constructed to investigate the role of sclerostin in HDPCs senescence and senescence-related impairment of odontoblastic differentiation potential. Results By immunohistochemistry and qRT-PCR, we found a significantly increased expression level of sclerostin in senescent human dental pulp compared with that of young human dental pulp. Additionally, elevated sclerostin expression was found in subculture-induced senescent HDPCs in vitro. By sclerostin overexpression and knockdown, we found that sclerostin promoted HDPCs senescence-related decline of proliferation and odontoblastic differentiation potential with increased expression of p16, p53 and p21 and downregulation of the Wnt signaling pathway. Discussion The increased expression of sclerostin is responsible for the decline of proliferation and odontoblastic differentiation potential of HDPCs during cellular senescence. Anti-sclerostin treatment may be beneficial for the maintenance of the proliferation and odontoblastic differentiation potentials of HDPCs.

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