Role of the Extracellular Signal-regulated Kinase 1/2 Pathway in Driving Tricalcium Silicate–induced Proliferation and Biomineralization of Human Dental Pulp Cells In Vitro

2013 ◽  
Vol 39 (8) ◽  
pp. 1023-1029 ◽  
Author(s):  
Rong Du ◽  
Tiantian Wu ◽  
Wenjuan Liu ◽  
Lifen Li ◽  
Long Jiang ◽  
...  
1997 ◽  
Vol 1 (3) ◽  
pp. 131-140 ◽  
Author(s):  
L. Stanislawski ◽  
J. P. Carreau ◽  
M. Pouchelet ◽  
Z. H. J. Chen ◽  
M. Goldberg

PeerJ ◽  
2018 ◽  
Vol 6 ◽  
pp. e5808 ◽  
Author(s):  
Yanjing Ou ◽  
Yi Zhou ◽  
Shanshan Liang ◽  
Yining Wang

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.


2020 ◽  
Vol 2020 ◽  
pp. 1-18 ◽  
Author(s):  
Xiangfen Li ◽  
Liu Wang ◽  
Qin Su ◽  
Ling Ye ◽  
Xuedong Zhou ◽  
...  

Human dental pulp cells (HDPCs) play a vital role in dentin formation and reparative dentinogenesis, which indicated their potential application in regenerative medicine. However, HDPCs, which can only be obtained from scarce human pulp tissues, also have a limited lifespan in vitro, and stem cells usually lose their original characteristics over a large number of passages. To overcome these challenges, we successfully immortalized human dental pulp cells using the piggyBac system which was employed to efficiently overexpress the SV40 T-Ag, and we then comprehensively described the cell biological behavior. The immortalized human dental pulp cells (iHDPCs) acquired long-term proliferative activity and expressed most HDPC markers. The iHDPCs maintained multiple differentiation potential and could be induced to differentiate into chondrogenic, osteogenic, and adipogenic cells in vitro. We also proved that the iHDPCs gained a stronger ability to migrate than the primary cells, while apoptosis was inhibited. Furthermore, highly proliferative iHDPCs displayed no oncogenicity when subcutaneously implanted into athymic nude mice. Finally, iHDPCs exhibited odontogenic differentiation ability and secreted dentin sialophosphoprotein (DSPP) when combined with a beta-tricalcium phosphate scaffold and bone morphogenetic protein-2 (BMP2) in vivo. Conclusively, the established iHDPCs are a valuable resource for mechanistic study of dental pulp cell differentiation and dental pulp injury repair, as well as for applications in tooth regeneration.


2013 ◽  
Vol 47 (6) ◽  
pp. 534-541 ◽  
Author(s):  
D. S. Kim ◽  
Y. S. Kim ◽  
W. J. Bae ◽  
H. J. Lee ◽  
S. W. Chang ◽  
...  

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Yoo-Jin Ko ◽  
Kil-Young Kwon ◽  
Kee-Yeon Kum ◽  
Woo-Cheol Lee ◽  
Seung-Ho Baek ◽  
...  

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.


Sign in / Sign up

Export Citation Format

Share Document