Dataset Information

CCK regulates osteogenic differentiation through TNFα/NF-κB in peri-implantitis.

ABSTRACT:

Objective

Peri-implantitis is characterized by peri-implant mucositis and alveolar bone resorption. This study investigated cholecystokinin (CCK) expression and the mechanism underlying its involvement in peri-implantitis.

Methods

mRNA sequencing was performed using the Gene Expression Omnibus database GSE106090. Human bone marrow mesenchymal stem cells (hBMSCs) were pretreated with various concentrations of CCK (0, 10, 30, or 100 nM) for 1 hour before induction in osteogenic differentiation medium for 2 weeks. Alkaline phosphatase (ALP) activity was determined, and the cells were stained with alizarin red. The expression levels of TNFα and the osteogenic markers ALP, RUNX2, and OCN were measured using quantitative real-time PCR. TNFα, phosphorylated P65, and total P65 levels were determined by western blot.

Results

Compared with healthy individuals, 262 and 215 genes were up- and down-regulated, respectively, in the periodontal tissues of patients with peri-implantitis. CCK expression was significantly upregulated in patients with peri-implantitis. CCK reduced ALP activity, osteogenic differentiation, and levels of the osteogenic markers ALP, RUNX2, and OCN. Moreover, CCK promoted levels of TNFα and phosphorylated P65, which is a marker of activation for the NF-κB inflammatory pathway.

Conclusions

CCK regulates osteogenic differentiation through the TNFα/NF-κB axis in peri-implantitis.

SUBMITTER: Chou L

PROVIDER: S-EPMC9747886 | biostudies-literature | 2022 Dec

REPOSITORIES: biostudies-literature

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Publications

CCK regulates osteogenic differentiation through TNFα/NF-κB in peri-implantitis.

Chou LongHang L Chang YaTing Y Lan KaiWen K Liu Meng M Lu YuKun Y Li XiaoLei X Li PeiRu P Xu Yue Y Xu Yue Y

The Journal of international medical research 20221201 12

<h4>Objective</h4>Peri-implantitis is characterized by peri-implant mucositis and alveolar bone resorption. This study investigated cholecystokinin (<i>CCK</i>) expression and the mechanism underlying its involvement in peri-implantitis.<h4>Methods</h4>mRNA sequencing was performed using the Gene Expression Omnibus database GSE106090. Human bone marrow mesenchymal stem cells (hBMSCs) were pretreated with various concentrations of CCK (0, 10, 30, or 100 nM) for 1 hour before induction in osteogen ...[more]

PMID: 36495169

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Project description:IntroductionMesenchymal stem cells (MSCs) have the ability to repair and regenerate tissue, home to sites of inflammation, and evade the host immune system. As such, they represent an attractive therapy for the treatment of autoimmune inflammatory diseases. However, results from in vivo murine studies in inflammatory arthritis have been conflicting, and this may be due to the genetic background of the MSCs used. It is known that the inflammatory milieu may influence properties of MSCs and that, in the case of human bone marrow-derived MSCs, this may be mediated by the nuclear factor-kappa-B (NF-κB) pathway. We sought to determine whether pro-inflammatory cytokines altered the differentiation and migration capacity of murine MSCs from different mouse strains and whether this was mediated by NF-κB.MethodsThe differentiation and migration of FVB and BALB/c MSCs were carried out in the presence of varying concentrations of tumor necrosis factor-alpha (TNFα) and interleukin (IL)-1β, and the NF-κB pathway was inhibited in one of two ways: either by transduction of MSCs with an adenoviral vector expressing a super-repressor of NF-κB or by the addition of curcumin to culture media.ResultsBoth BALB/c and FVB MSCs were sensitive to the effect of pro-inflammatory cytokines in vitro. TNFα and IL-1β suppressed BALB/c osteogenesis and adipogenesis and FVB osteogenesis. The migration of both cell types toward media containing fetal bovine serum was augmented by pre-stimulation with either cytokine. In neither cell type were the cytokine effects reversed by abrogation of the NF-κB pathway.ConclusionsThese data show that murine MSCs from different genetic backgrounds may be influenced by an inflammatory milieu in a manner that is not mediated by NF-κB, as is the case for human MSCs. This is not mediated by NF-κB. These findings are important and should influence how in vivo trials of murine MSCs are interpreted and the future development of pre-clinical studies in inflammatory diseases.

Dataset Information

CCK regulates osteogenic differentiation through TNFα/NF-κB in peri-implantitis.

Objective

Methods

Results

Conclusions

Publications

CCK regulates osteogenic differentiation through TNFα/NF-κB in peri-implantitis.

Similar Datasets

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