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Effect of TNF‑α on the proliferation and osteogenesis of human periodontal mesenchymal stem cells
Author(s) -
Yiting Cao,
Yiwei Wang,
Chenlin Li,
Qian Jiang,
Laikuan Zhu
Publication year - 2021
Publication title -
experimental and therapeutic medicine
Language(s) - English
Resource type - Journals
eISSN - 1792-1015
pISSN - 1792-0981
DOI - 10.3892/etm.2021.9851
Subject(s) - runx2 , alkaline phosphatase , periodontal ligament stem cells , mesenchymal stem cell , bone sialoprotein , microbiology and biotechnology , osteocalcin , chemistry , tumor necrosis factor alpha , biology , immunology , biochemistry , enzyme
The aim of the present study was to investigate the effect of tumor necrosis factor-α (TNF-α) on the proliferation and osteogenesis of human periodontal mesenchymal stem cells (hPDLSCs). Antigen expression in hPDLSCs was detected by flow cytometry. hPDLSCs were divided into four groups: A control group with no TNF-α treatment, and three experimental groups treated with 0.1, 1 and 10 ng/ml TNF-α, respectively. The effect of TNF-α on proliferation of hPDLSCs in vitro was detected using a Cell Counting Kit-8 assay. Differentiation into an osteogenic lineage was detected by alkaline phosphatase sand alizarin red staining, and the mRNA and protein expression levels of runt-related transcription factor 2 (Runx2), osteocalcin (OCN) and type I collagen (Col-I) were detected using reverse transcription-quantitative PCR and western blot respectively. Following treatment with 10 ng/ml TNF-α, proliferation was significantly increased compared with an untreated control group (P<0.01). Additionally, there was a significant inhibition of alkaline phosphatase enzyme activity, alizarin red mineralization node size, and in the gene and protein expression levels of osteogenic differentiation markers, including Runx2, OCN and COL-I (all, P<0.05). Taken together, the results indicated that treatment with 10 ng/ml TNF-α promoted the proliferation of hPDLSCs in vitro and inhibited osteogenic differentiation of hPDLSCs, providing an experimental basis for regulation of hPDLSC-mediated periodontal tissue regeneration.

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