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 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.

Role of Protein Phosphatase 1 in Angiogenesis and Odontoblastic Differentiation of Human Dental Pulp Cells

2017 ◽  
Vol 43 (3) ◽  
pp. 417-424 ◽  
Author(s):  
Ji-Youn Kim ◽  
Duk-Su Kim ◽  
Q-Schick Auh ◽  
Jin-Kyu Yi ◽  
Sung Ung Moon ◽  
...  
Keyword(s):  
Protein Phosphatase ◽  
Dental Pulp ◽  
Protein Phosphatase 1 ◽  
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.

scholarly journals The Anti-Inflammatory Effect of Human Telomerase-Derived Peptide onP. gingivalisLipopolysaccharide-Induced Inflammatory Cytokine Production and Its Mechanism in Human Dental Pulp Cells

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Yoo-Jin Ko ◽  
Kil-Young Kwon ◽  
Kee-Yeon Kum ◽  
Woo-Cheol Lee ◽  
Seung-Ho Baek ◽  
...  
Keyword(s):  
Dental Pulp ◽  
Map Kinases ◽  
Inhibitory Effect ◽  
Dental Pulp Cells ◽  
Human Dental Pulp Cells ◽  
Human Dental Pulp ◽  
Pulp Cells ◽  
Anti Inflammatory ◽  
Human Telomerase

Porphyromonas gingivalisis considered with inducing pulpal inflammation and has lipopolysaccharide (LPS) as an inflammatory stimulator. GV1001 peptide has anticancer and anti-inflammation activity due to inhibiting activation of signaling molecules after penetration into the various types of cells. Therefore, this study examined inhibitory effect of GV1001 on dental pulp cells (hDPCs) stimulated byP. gingivalisLPS. The intracellular distribution of GV1001 was analyzed by confocal microscopy. Real-time RT-PCR was performed to determine the expression levels of TNF-αand IL-6 cytokines. The role of signaling by MAP kinases (ERK and p38) was explored using Western blot analysis. The effect of GV1001 peptide on hDPCs viability was measured by MTT assay. GV1001 was predominantly located in hDPC cytoplasm. The peptide inhibitedP. gingivalisLPS-induced TNF-αand IL-6 production in hDPCs without significant cytotoxicity. Furthermore, GV1001 treatment markedly inhibited the phosphorylation of MAP kinases (ERK and p38) in LPS-stimulated hDPCs. GV1001 may preventP. gingivalisLPS-induced inflammation of apical tissue. Also, these findings provide mechanistic insight into how GV1001 peptide causes anti-inflammatory actions in LPS-stimulated pulpitis without significantly affecting cell viability.

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