Jia, Xiaoshi; Xu, Hudi; Miron, Richard John; Yin, Chengcheng; Zhang, Xiaoxin; Wu, Min; Zhang, Yufeng (2018). EZH1 Is Associated with TCP-Induced Bone Regeneration through Macrophage Polarization. Stem cells international, 2018, p. 6310560. Hindawi 10.1155/2018/6310560
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Macrophages have been found to regulate the effects of biomaterials throughout the entire tissue repair process as an antigen-presenting cell. As a well-defined osteoconductive biomaterial for bone defect regeneration, tricalcium phosphate (TCP) has been found to facilitate a favourable osteoimmunomodulatory response that can shift macrophage polarization towards the M2 phenotype. In the present study, our group discovered that a histone methyltransferase enhancer of zeste1 (EZH1) was drastically downregulated in Thp1 cells stimulated by TCP, indicating that EZH1 may participate in the macrophage phenotype shifting. Furthermore, the NF-B pathway in macrophages was significantly downregulated through stimulation of TCP, suggesting a potential interaction between EZH1 and the NF-B pathway. Utilizing gene knock-down therapy in macrophages, it was found that depletion of EZH1 induced M2 macrophage polarization but did not downregulate NF-B. When the NF-B pathway was inhibited, the expression of EZH1 was significantly downregulated, suggesting that the inhibition of EZH1 may be regulated by the NF-B pathway. These novel findings provide valuable insights into a potential gene target system that controls M2 macrophage polarization which ultimately favours a microenvironment suitable for bone repair.
Item Type: |
Journal Article (Original Article) |
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Division/Institute: |
04 Faculty of Medicine > School of Dental Medicine > Department of Periodontology 04 Faculty of Medicine > School of Dental Medicine > Periodontics Research |
UniBE Contributor: |
Miron, Richard John |
Subjects: |
600 Technology > 610 Medicine & health |
ISSN: |
1687-966X |
Publisher: |
Hindawi |
Language: |
English |
Submitter: |
Doris Burri |
Date Deposited: |
18 Jul 2019 14:12 |
Last Modified: |
05 Dec 2022 15:25 |
Publisher DOI: |
10.1155/2018/6310560 |
PubMed ID: |
30228822 |
BORIS DOI: |
10.7892/boris.125319 |
URI: |
https://boris.unibe.ch/id/eprint/125319 |