Effects of beta-tricalcium phosphate particles on primary cultured murine dendritic cells and macrophages

Tai, Sachiko; Cheng, Jinyan; Ishii, Hidee; Shimono, Kasumi; Zangiacomi, Vincent; Satoh, Takatomo; Hosono, Tetsuji; Suzuki, Eiji; Yamaguchi, Ken; Maruyama, Kouji

doi:10.1016/j.intimp.2016.09.021

Cited by 13 publications

(15 citation statements)

References 32 publications

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“…In a study conducted by Chen et al, it was revealed that macrophage polarization was driven towards the M1 extreme when cobalt was incorporated into β -tricalcium phosphate and this negatively impacted the ability for bone-forming osteoblasts to contribute to new bone formation [ 11 ]. Similarly, a study by Tai et al found that TCP particles promoted macrophage expression of CD86, an M1 surface molecule in macrophages [ 12 ]. In contrast, however, a study by Chen et al found that TCP extracts facilitated a favourable osteoimmunomodulatory response that promoted M2 macrophage polarization including the release of bone morphogenetic protein-2 (BMP2), one of the best-known inducers of osteoblast differentiation of bone marrow stromal cells (BMSCs) [ 13 , 14 ].…”

Section: Introductionmentioning

confidence: 95%

EZH1 Is Associated with TCP-Induced Bone Regeneration through Macrophage Polarization

Jia

Miron

et al. 2018

Stem Cells International

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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-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.

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Section: Introductionmentioning

confidence: 95%

EZH1 Is Associated with TCP-Induced Bone Regeneration through Macrophage Polarization

Jia

Miron

et al. 2018

Stem Cells International

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“…This result is not unexpected, considering the fact that the scaffold surface is not in direct contact with the medium due to the cell layer covering the surface. However, β-TCP particles phenotypically and functionally stimulated DCs, including upregulated costimulatory molecules CD40, CD80, and CD86, and MHC class II and increased cytokines and chemokines M-CSF, CCL2, and CCL3 [52].…”

Section: Discussionmentioning

confidence: 99%

Jaw Periosteal Cells Seeded in Beta-Tricalcium Phosphate Inhibit Dendritic Cell Maturation

et al. 2020

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Mesenchymal stem cells (MSCs) have gained attraction not only in the field of regenerative medicine but also in the field of autoimmune disease therapies or organ transplantation due to their immunoregulatory and/or immunosuppressive features. Dendritic cells (DCs) play a crucial role in initiating and regulating immune reactions by promoting antigen-specific T cell activation. In this study, we investigated the effect of human jaw periosteal progenitor cells (JPCs) seeded in beta-tricalcium phosphate (β-TCP) scaffolds on monocyte-derived DC differentiation. Significantly lower numbers of differentiated DCs were observed in the presence of normal (Co) and osteogenically induced (Ob) JPCs-seeded β-TCP constructs. Gene expression analysis revealed significantly lower interleukin-12 subunit p35 (IL-12p35) and interleukin-12 receptor beta 2 (IL-12Rβ2) and pro-inflammatory cytokine interferon-gamma (IFN-γ) levels in DCs under Ob conditions, while interleukin-8 (IL-8) gene levels were significantly increased. Furthermore, in the presence of JPCs-seeded β-TCP constructs, interleukin-10 (IL-10) gene expression was significantly induced in DCs, particularly under Ob conditions. Analysis of DC protein levels shows that granulocyte-colony stimulating factor (G-CSF) was significantly upregulated in coculture groups. Our results indicate that undifferentiated and osteogenically induced JPCs-seeded β-TCP constructs have an overall inhibitory effect on monocyte-derived DC maturation.

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“…The b-TCP was initially colonized by neutrophils, followed by lymphocytes, histiocytes (macrophages), and fibroblasts, and finally by multinucleated giant cells. 6,26 Studies have reported that human peripheral blood mononuclear cells and J774A.1 cells (monocyte/macrophage cells derived from mice) incubated with b-TCP exhibited upregulation of the protein level of tumor necrosis factor alpha. 26,27 b-TCP also induced the protein level of macrophage inflammatory protein 1 alpha in J774A.1 cells.…”

Section: Histological Evaluationsmentioning

confidence: 99%

“…26 Both proteins are known to stimulate recruitment of various immune cells to the site of inflammation, thus upregulation of these proteins in the presence of b-TCP triggers and enhances the migration of a huge number of immune cells towards the area surrounding b-TCP in vivo. 6,26 The recruitment of these immune cell types to the vicinity of b-TCP lead to degradation of b-TCP via phagocytosis. Eggli et al found a cluster of macrophages packed with granular b-TCP on the implantation site in a rabbit model, which suggests that macrophages may play an active role in intracellular degradation of small detached ceramic particles.…”

Section: Histological Evaluationsmentioning

confidence: 99%

“…β-TCP mimics the major natural inorganic component of bone 1,2 and is bioactive, biodegradable, and osteoconductive. 3 –9 It serves as a template for bone cell attachment, proliferation, migration, and phenotypic expression, leading to the formation of new bone. 10 –12 Moreover, toxicity assessment has shown that β-TCP is a safe and biocompatible biomaterial.…”

Section: Introductionmentioning

confidence: 99%

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In vivo efficacy and toxicity of synthesized nano-β-tricalcium phosphate in a rabbit tibial defect model

Ooi

Kasim

Shaari

et al. 2018

Toxicology Research and Application

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Previous studies of the biocompatibility of b-tricalcium phosphate (b-TCP) focused on bulk-sized b-TCP, and little is known about the biocompatibility of nano b-TCP particles (nb-TCP). The objectives of this study were to synthesize nb-TCP particles and determine their efficacy in a rabbit tibial defect model. The nb-TCP particles were first synthesized using a wet chemical precipitation process. The particles were then implanted in the left tibia of New Zealand white rabbits, and the defect site healing was evaluated for a period of 16 weeks using radiography, computed tomography, and histology. Data were compared with those of a sham (empty) control. Results showed that the defect site treated with nb-TCP particles did not heal completely after 16 weeks, whereas full cortical bone recovery was observed in the sham control group of rabbits. Histopathological examination showed that the nb-TCP particles caused an excessive and prolonged inflammatory response by the host. The nano-scaled size and biodegradability of the synthesized nb-TCP particles may have been responsible for this progressive and extended inflammatory response, which delayed the bone healing process. The underlying mechanism for this effect remains unclear and warrants further investigation.

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Effects of beta-tricalcium phosphate particles on primary cultured murine dendritic cells and macrophages

Cited by 13 publications

References 32 publications

EZH1 Is Associated with TCP-Induced Bone Regeneration through Macrophage Polarization

EZH1 Is Associated with TCP-Induced Bone Regeneration through Macrophage Polarization

Jaw Periosteal Cells Seeded in Beta-Tricalcium Phosphate Inhibit Dendritic Cell Maturation

In vivo efficacy and toxicity of synthesized nano-β-tricalcium phosphate in a rabbit tibial defect model

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