期刊
BIOMEDICINE & PHARMACOTHERAPY
卷 114, 期 -, 页码 -出版社
ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
DOI: 10.1016/j.biopha.2019.108803
关键词
Stem cells from human exfoliated deciduous teeth; Co-Culture; Osteoclastogenesis; Inflammatory microenvironment; Nuclear factor-kappa B
资金
- National Natural Science Foundation of China [81701018, 8150030603]
- International Science and Technology Cooperation Projects [2015-TSYS-2028]
- Clinical research support foundation of General Hospital of Chinese PLA [2017 FC-TSYS-3013]
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-kappa B (NF-kappa B) 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-alpha (TNF-alpha) was significantly higher in SHED than in DPSCs. Expression of cathepsin K (CTSK), TRAP, and receptor-activator of nuclear-factor-kappa B ligand (RANKL), RANKL/osteoprotegerin (OPG) ratio, and expression of cytoplasmic phosphorylated inhibitor of NF-kappa B alpha (p-I kappa B alpha) and nuclear p65 were markedly up-regulated in SHED post the TNF-alpha treatment but decreased following NF-kappa B inhibition. In conclusion, inflammatory cytokine TNF-alpha appeared to activate NF-kappa B pathway to up-regulate expression of NF-kappa B, enhancing ability of SHED in promoting osteoclastogenesis via regulating RANKL/OPG expression.
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