scholarly journals Alcohol Inhibits Odontogenic Differentiation of Human Dental Pulp Cells by Activating mTOR Signaling

2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
Wei Qin ◽  
Qi-Ting Huang ◽  
Michael D. Weir ◽  
Zhi Song ◽  
Ashraf F. Fouad ◽  
...  
Keyword(s):  
Behavioral Problems ◽  
Dental Pulp ◽  
Nodule Formation ◽  
Dependent Manner ◽  
Dental Pulp Cells ◽  
Human Dental Pulp Cells ◽  
Odontoblastic Differentiation ◽  
Heavy Alcohol Consumption ◽  
Human Dental Pulp ◽  
Pulp Cells

Long-term heavy alcohol consumption could result in a range of health, social, and behavioral problems. People who abuse alcohol are at high risks of seriously having osteopenia, periodontal disease, and compromised oral health. However, the role of ethanol (EtOH) in the biological functions of human dental pulp cells (DPCs) is unknown. Whether EtOH affects the odontoblastic differentiation of DPCs through the mechanistic target of rapamycin (mTOR) remains unexplored. The objective of this study was to investigate the effects of EtOH on DPC differentiation and mineralization. DPCs were isolated and purified from human dental pulps. The proliferation and odontoblastic differentiation of DPCs treated with EtOH were subsequently investigated. Different doses of EtOH were shown to be cytocompatible with DPCs. EtOH significantly activated the mTOR pathway in a dose-dependent manner. In addition, EtOH downregulated the alkaline phosphatase activity, attenuated the mineralized nodule formation, and suppressed the expression of odontoblastic markers including ALP, DSPP, DMP-1, Runx2, and OCN. Moreover, the pretreatment with rapamycin, a specific mTOR inhibitor, markedly reversed the EtOH-induced odontoblastic differentiation and cell mineralization. Our findings show for the first time that EtOH can suppress DPC differentiation and mineralization in a mTOR-dependent manner, indicating that EtOH may be involved in negatively regulating the dental pulp repair.

Baicalein Promotes Angiogenesis and Odontoblastic Differentiation via the BMP and Wnt Pathways in Human Dental Pulp Cells

2016 ◽  
Vol 44 (07) ◽  
pp. 1457-1472 ◽  
Author(s):  
Sang-Im Lee ◽  
Sun-Young Kim ◽  
Kyung-Ran Park ◽  
Eun-Cheol Kim
Keyword(s):  
Dental Pulp ◽  
Marker Genes ◽  
Signal Pathways ◽  
Dependent Manner ◽  
Dental Pulp Cells ◽  
Alizarin Red ◽  
Human Dental Pulp Cells ◽  
Odontoblastic Differentiation ◽  
Human Dental Pulp ◽  
Pulp Cells

Baicalein is an active flavonoid extracted from the root of Scutellaria baicalensis that has anticancer and anti-inflammatory properties; its effects on osteoblastic and angiogenic potential are controversial. The aim of this study was to investigate the effects of baicalein on odontoblastic differentiation and angiogenesis and the underlying mechanism in human dental pulp cells (HDPCs). Baicalein (1–10[Formula: see text][Formula: see text]M) had no cytotoxic effects and promoted alkaline phosphatase (ALP) activity, mineralization assayed by Alizarin Red-S staining, and the mRNA expression of marker genes, in a concentration-dependent manner. In addition, baicalein upregulated angiogenic factors and increased in vitro capillary-like tube formation. Moreover, baicalein upregulated bone morphogenetic protein (BMP)-2 mRNA and phosphorylation of Smad 1/5/8 and Wnt ligand mRNA, glycogen synthase kinase-3, and nuclear [Formula: see text]-catenin. The odontogenic and angiogenic effects of baicalein were abolished by the BMP antagonist noggin and the Wnt/[Formula: see text]-catenin receptor antagonist DKK-1. These results demonstrate that baicalein promoted odontoblastic differentiation and angiogenesis of HDPCs by activating the BMP and Wnt/[Formula: see text]-catenin signal pathways. Our findings suggest that baicalein may contribute to dental pulp repair and regenerative endodontics.

scholarly journals Sclerostin promotes human dental pulp cells senescence

PeerJ ◽  
2018 ◽  
Vol 6 ◽  
pp. e5808 ◽  
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.

The role of SDF-1 and CXCR4 on odontoblastic differentiation in human dental pulp cells

2013 ◽  
Vol 47 (6) ◽  
pp. 534-541 ◽  
Author(s):  
D. S. Kim ◽  
Y. S. Kim ◽  
W. J. Bae ◽  
H. J. Lee ◽  
S. W. Chang ◽  
...  
Keyword(s):  
Dental Pulp ◽  
Dental Pulp Cells ◽  
Human Dental Pulp Cells ◽  
Odontoblastic Differentiation ◽  
Human Dental Pulp ◽  
Pulp Cells

scholarly journals Lipopolysaccharide stimulation improves the odontoblastic differentiation of human dental pulp cells

2014 ◽  
Vol 11 (5) ◽  
pp. 3547-3552 ◽  
Author(s):  
YIHUA HUANG ◽  
HONGWEI JIANG ◽  
QIMEI GONG ◽  
XUYAN LI ◽  
JUNQI LING
Keyword(s):  
Dental Pulp ◽  
Dental Pulp Cells ◽  
Human Dental Pulp Cells ◽  
Odontoblastic Differentiation ◽  
Human Dental Pulp ◽  
Pulp Cells

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

2015 ◽  
Vol 93 (6) ◽  
pp. 587-595 ◽  
Author(s):  
Su Mi Woo ◽  
Kyung Joo Seong ◽  
Sang Jin Oh ◽  
Hong Ju Park ◽  
Sun Hun Kim ◽  
...  
Keyword(s):  
Dental Pulp ◽  
Mapk Pathway ◽  
Mapk Signaling ◽  
Dental Pulp Cells ◽  
Human Dental Pulp Cells ◽  
Odontoblastic Differentiation ◽  
Alp Activity ◽  
Human Dental Pulp ◽  
Pulp Cells ◽  
17Β Estradiol

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.

Calcium-sensing receptor-ERK signaling promotes odontoblastic differentiation of human dental pulp cells

Bone ◽  
2017 ◽  
Vol 101 ◽  
pp. 191-201 ◽  
Author(s):  
Hiroyuki Mizumachi ◽  
Shinichiro Yoshida ◽  
Atsushi Tomokiyo ◽  
Daigaku Hasegawa ◽  
Sayuri Hamano ◽  
...  
Keyword(s):  
Dental Pulp ◽  
Erk Signaling ◽  
Dental Pulp Cells ◽  
Calcium Sensing Receptor ◽  
Human Dental Pulp Cells ◽  
Odontoblastic Differentiation ◽  
Calcium Sensing ◽  
Human Dental Pulp ◽  
Pulp Cells
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