Sclerostin promotes human dental pulp cells senescence

Bibliographic Details
Title: Sclerostin promotes human dental pulp cells senescence
Authors: Yanjing Ou, Yi Zhou, Shanshan Liang, Yining Wang
Source: PeerJ, Vol 6, p e5808 (2018)
Publisher Information: PeerJ Inc., 2018.
Publication Year: 2018
Collection: LCC:Medicine
LCC:Biology (General)
Subject Terms: Sclerostin, Human dental pulp cell, Senescence, p21, p16, p53, Medicine, Biology (General), QH301-705.5
More Details: 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.
Document Type: article
File Description: electronic resource
Language: English
ISSN: 2167-8359
Relation: https://peerj.com/articles/5808.pdf; https://peerj.com/articles/5808/; https://doaj.org/toc/2167-8359
DOI: 10.7717/peerj.5808
Access URL: https://doaj.org/article/1676fd4e18ab4a349b3e6651568cd375
Accession Number: edsdoj.1676fd4e18ab4a349b3e6651568cd375
Database: Directory of Open Access Journals
More Details
ISSN:21678359
DOI:10.7717/peerj.5808
Published in:PeerJ
Language:English