Format

Send to

Choose Destination
Biomed Pharmacother. 2019 Jun;114:108803. doi: 10.1016/j.biopha.2019.108803. Epub 2019 Apr 2.

Effect of tumor necrosis factor α on ability of SHED to promote osteoclastogenesis during physiological root resorption.

Author information

1
Department of Stomatology, Eight Medical Center,General Hospital of Chinese PLA, Beijing 100853, China.
2
Department of Orthodontics, First Medical Center, General Hospital of Chinese PLA, Beijing 100091, China.
3
Department of Orthodontics, First Medical Center, General Hospital of Chinese PLA, Beijing 100091, China. Electronic address: xululu1977@163.com.

Abstract

Physiological root resorption of deciduous teeth is a normal phenomenon, however, the potential mechanisms underlying this process remain unclear. This study aimed to investigate ability of stem cells from human exfoliated deciduous teeth (SHED) on promoting the osteoclastic differentiation of osteoclast precursors and clarify mechanisms underlying this process in vitro. SHED and dental pulp stem cells (DPSCs) were obtained from deciduous teeth and healthy permanent teeth. An indirect co-culture system of SHED or DPSCs were used. The osteoclast precursor peripheral blood mononuclear cells (PBMCs) were established. Ability of SHED and DPSCs in promoting osteoclastogenesis was determined using triiodothyronine receptor auxiliary protein (TRAP) staining, real-time real-time PCR (RT-PCR) and western blotting. The effect of inflammation on the pro-osteoclastogenesis ability of SHED was determined using enzyme linked immunosorbent assay (ELISA), RT-PCR and western blotting. The function of the nuclear factor-κB (NF-κB) pathway in promoting the osteoclastogenesis ability of SHED was determined using RT-PCR and western blotting. SHED exhibited an increased ability to promote osteoclastic differentiation. Expression of tumor necrosis factor-α (TNF-α) was significantly higher in SHED than in DPSCs. Expression of cathepsin K (CTSK), TRAP, and receptor-activator of nuclear-factor-κ B ligand (RANKL), RANKL/osteoprotegerin (OPG) ratio, and expression of cytoplasmic phosphorylated inhibitor of NF-κB α (p-IκBα) and nuclear p65 were markedly up-regulated in SHED post the TNF-α treatment but decreased following NF-κB inhibition. In conclusion, inflammatory cytokine TNF-α appeared to activate NF-κB pathway to up-regulate expression of NF-κB, enhancing ability of SHED in promoting osteoclastogenesis via regulating RANKL/OPG expression.

KEYWORDS:

Co-Culture; Inflammatory microenvironment; Nuclear factor-κB; Osteoclastogenesis; Stem cells from human exfoliated deciduous teeth

PMID:
30951949
DOI:
10.1016/j.biopha.2019.108803
Free full text

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center