EZH1 Is Associated with TCP-Induced Bone Regeneration through Macrophage Polarization
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 osteoimmunom...
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| Main Authors: | , , , , , , |
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| Format: | Article |
| Language: | English |
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Wiley
2018-01-01
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| Series: | Stem Cells International |
| Online Access: | http://dx.doi.org/10.1155/2018/6310560 |
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| author | Xiaoshi Jia Hudi Xu Richard J. Miron Chengcheng Yin Xiaoxin Zhang Min Wu Yufeng Zhang |
| author_facet | Xiaoshi Jia Hudi Xu Richard J. Miron Chengcheng Yin Xiaoxin Zhang Min Wu Yufeng Zhang |
| author_sort | Xiaoshi Jia |
| collection | DOAJ |
| description | 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-κB pathway in macrophages was significantly downregulated through stimulation of TCP, suggesting a potential interaction between EZH1 and the NF-κB pathway. Utilizing gene knock-down therapy in macrophages, it was found that depletion of EZH1 induced M2 macrophage polarization but did not downregulate NF-κB. When the NF-κB pathway was inhibited, the expression of EZH1 was significantly downregulated, suggesting that the inhibition of EZH1 may be regulated by the NF-κB 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. |
| format | Article |
| id | doaj-art-2256e894a1424074bd10722d365da3df |
| institution | OA Journals |
| issn | 1687-966X 1687-9678 |
| language | English |
| publishDate | 2018-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Stem Cells International |
| spelling | doaj-art-2256e894a1424074bd10722d365da3df2025-08-20T02:04:06ZengWileyStem Cells International1687-966X1687-96782018-01-01201810.1155/2018/63105606310560EZH1 Is Associated with TCP-Induced Bone Regeneration through Macrophage PolarizationXiaoshi Jia0Hudi Xu1Richard J. Miron2Chengcheng Yin3Xiaoxin Zhang4Min Wu5Yufeng Zhang6The State Key Laboratory Breeding Base of Basic Science of Stomatology (Hubei-MOST) and Key Laboratory of Oral Biomedicine Ministry of Education, Wuhan University, Wuhan, ChinaThe State Key Laboratory Breeding Base of Basic Science of Stomatology (Hubei-MOST) and Key Laboratory of Oral Biomedicine Ministry of Education, Wuhan University, Wuhan, ChinaDepartment of Periodontology, University of Bern, Bern, SwitzerlandThe State Key Laboratory Breeding Base of Basic Science of Stomatology (Hubei-MOST) and Key Laboratory of Oral Biomedicine Ministry of Education, Wuhan University, Wuhan, ChinaThe State Key Laboratory Breeding Base of Basic Science of Stomatology (Hubei-MOST) and Key Laboratory of Oral Biomedicine Ministry of Education, Wuhan University, Wuhan, ChinaHubei Key Laboratory of Cell Homeostasis, Hubei Key Laboratory of Developmentally Originated Disease, Department of Biochemistry and Molecular Biology, College of Life Sciences, Wuhan University, Wuhan, Hubei 430072, ChinaThe State Key Laboratory Breeding Base of Basic Science of Stomatology (Hubei-MOST) and Key Laboratory of Oral Biomedicine Ministry of Education, Wuhan University, Wuhan, ChinaMacrophages 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-κB pathway in macrophages was significantly downregulated through stimulation of TCP, suggesting a potential interaction between EZH1 and the NF-κB pathway. Utilizing gene knock-down therapy in macrophages, it was found that depletion of EZH1 induced M2 macrophage polarization but did not downregulate NF-κB. When the NF-κB pathway was inhibited, the expression of EZH1 was significantly downregulated, suggesting that the inhibition of EZH1 may be regulated by the NF-κB 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.http://dx.doi.org/10.1155/2018/6310560 |
| spellingShingle | Xiaoshi Jia Hudi Xu Richard J. Miron Chengcheng Yin Xiaoxin Zhang Min Wu Yufeng Zhang EZH1 Is Associated with TCP-Induced Bone Regeneration through Macrophage Polarization Stem Cells International |
| title | EZH1 Is Associated with TCP-Induced Bone Regeneration through Macrophage Polarization |
| title_full | EZH1 Is Associated with TCP-Induced Bone Regeneration through Macrophage Polarization |
| title_fullStr | EZH1 Is Associated with TCP-Induced Bone Regeneration through Macrophage Polarization |
| title_full_unstemmed | EZH1 Is Associated with TCP-Induced Bone Regeneration through Macrophage Polarization |
| title_short | EZH1 Is Associated with TCP-Induced Bone Regeneration through Macrophage Polarization |
| title_sort | ezh1 is associated with tcp induced bone regeneration through macrophage polarization |
| url | http://dx.doi.org/10.1155/2018/6310560 |
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