Mineral trioxide aggregate enhances the osteogenic capacity of periodontal ligament stem cells via NF‐κB and MAPK signaling pathways

Journal of Cellular Physiology - Tập 233 Số 3 - Trang 2386-2397 - 2018
Yanqiu Wang1, Yixiang Zhou2,1, Jin Lin1, Xiyao Pang1, Yadie Lu1, Zilu Wang1, Yu Yan1, Jinhua Yu1
1Key Laboratory of Oral Diseases of Jiangsu Province and Stomatological Institute of Nanjing Medical University, Nanjing, Jiangsu, China
2IVY Dental Clinic, Hangzhou, Zhejiang, China

Tóm tắt

Mineral trioxide aggregate (MTA), as a bioactive material, has a widespread application in clinical practice. To date, the effects of MTA on the proliferation and differentiation of human periodontal ligament stem cells (hPDLSCs) remain unclear. hPDLSCs were isolated from human periodontal ligament tissues and cultured with MTA conditioned media. Cell counting kit‐8 (CCK‐8) assay was performed to assess the proliferation capacity of MTA‐treated hPDLSCs. Immunofluorescence assay, alkaline phosphatase (ALP) activity, alizarin red staining, real‐time RT‐PCR, and western blot analyses were used to investigate the odonto/osteogenic capacity of hPDLSCs as well as the involvement of NF‐κB and MAPK pathways. ALP activity assay revealed that 2 mg/ml was the optimal concentration for the induction of hPDLSCs by MTA. The protein expression of DSP, RUNX2, OCN, OSX, OPN, DMP1, ALP, and COL‐I in MTA‐treated hPDLSCs was significantly higher than those in control group (p < 0.01). When hPDLSCs were treated with the inhibitors of NF‐κB and MAPK pathways (U0126, SP600125, SB203580, and BMS345541), the effects of MTA on the differentiation of hPDLSCs were suppressed. Mechanistically, P65 was detected to transfer from cytoplasm to nuclei, as indicated by western blot and immunofluorescence assay. Moreover, MAPK‐related proteins and its downstream transcription factors were also upregulated in MTA‐treated hPDLSCs. Together, mineral trioxide aggregate can promote the odonto/osteogenic capacity of hPDLSCs via activating the NF‐κB and MAPK pathways.

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Thông tin xuất bản

Journal of Cellular Physiology

Tập 233 Số 3

2386-2397

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