Molecular determinants for the polarization of macrophage and osteoclast

Yang, Dengbao; Wan, Yihong

doi:10.1007/s00281-019-00754-3

Cited by 67 publications

(55 citation statements)

References 159 publications

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“…The TME consists of various types of cells mediating the communication between malignant cells, immune cells and stromal cells 79 . TAMs, especially the M2-TAMs relatively express high CD206 and MRC1 , and play critical roles in tumor growth, angiogenesis, invasion and metastasis especially 80 . In the present study, we identified three distinct TAM populations in OS, and the majority TAMs were M2.…”

Section: Discussionmentioning

confidence: 99%

Single-cell RNA landscape of intratumoral heterogeneity and immunosuppressive microenvironment in advanced osteosarcoma

et al. 2020

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Osteosarcoma is the most frequent primary bone tumor with poor prognosis. Through RNA-sequencing of 100,987 individual cells from 7 primary, 2 recurrent, and 2 lung metastatic osteosarcoma lesions, 11 major cell clusters are identified based on unbiased clustering of gene expression profiles and canonical markers. The transcriptomic properties, regulators and dynamics of osteosarcoma malignant cells together with their tumor microenvironment particularly stromal and immune cells are characterized. The transdifferentiation of malignant osteoblastic cells from malignant chondroblastic cells is revealed by analyses of inferred copy-number variation and trajectory. A proinflammatory FABP4+ macrophages infiltration is noticed in lung metastatic osteosarcoma lesions. Lower osteoclasts infiltration is observed in chondroblastic, recurrent and lung metastatic osteosarcoma lesions compared to primary osteoblastic osteosarcoma lesions. Importantly, TIGIT blockade enhances the cytotoxicity effects of the primary CD3+ T cells with high proportion of TIGIT+ cells against osteosarcoma. These results present a single-cell atlas, explore intratumor heterogeneity, and provide potential therapeutic targets for osteosarcoma.

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Section: Discussionmentioning

confidence: 99%

Single-cell RNA landscape of intratumoral heterogeneity and immunosuppressive microenvironment in advanced osteosarcoma

et al. 2020

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“…17 M1 macrophages are induced by interferon-γ or lipopolysaccharide, and secrete pro-inflammatory cytokines including interleukin-1β (IL-1β), inducible nitric oxide synthase (iNOS), tumor necrosis factor α (TNF-α) and reactive oxygen species (ROS), to promote inflammation and impair implants. In contrast, M2 macrophages are induced by cytokines IL-4 and IL-10, 18,19 and secrete anti-inflammatory cytokines such as IL-10, along with various growth factors such as transforming growth factor β (TGF-β), vascular endothelial growth factor (VEGF), 1,25-dihydroxy vitamin D3 and bone morphogenetic protein (BMP) to suppress inflammation, promote extracellular matrix reconstruction and bone healing. [20][21][22] Recent studies have shown that the presence of chronic M1 macrophage at the bone-implant interface inhibited new bone formation and promoted implant inflammatory encapsulation.…”

Section: Introductionmentioning

confidence: 99%

<p>Improved Immunoregulation of Ultra-Low-Dose Silver Nanoparticle-Loaded TiO<sub>2</sub> Nanotubes via M2 Macrophage Polarization by Regulating GLUT1 and Autophagy</p>

Chen¹,

Guan²,

Ren³

et al. 2020

IJN

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Introduction: The bone regeneration of endosseous implanted biomaterials is often impaired by the host immune response, especially macrophage-related inflammation which plays an important role in the bone healing process. Thus, it is a promising strategy to design an osteo-immunomodulatory biomaterial to take advantage of the macrophage-related immune response and improve the osseointegration performance of the implant. Methods: In this study, we developed an antibacterial silver nanoparticle-loaded TiO 2 nanotubes (Ag@TiO 2-NTs) using an electrochemical anodization method to make the surface modification and investigated the influences of Ag@TiO 2-NTs on the macrophage polarization, osteo-immune microenvironment as well as its potential molecular mechanisms in vitro and in vivo. Results: The results showed that Ag@TiO 2-NTs with controlled releasing of ultra-low-dose Ag + ions had the excellent ability to induce the macrophage polarization towards the M2 phenotype and create a suitable osteo-immune microenvironment in vitro, via inhibiting PI3K/Akt, suppressing the downstream effector GLUT1, and activating autophagy. Moreover, Ag@TiO 2-NTs surface could improve bone formation, suppress inflammation, and promote osteo-immune microenvironment compared to the TiO 2-NTs and polished Ti surfaces in vivo. These findings suggested that Ag@TiO 2-NTs with controlled releasing of ultra-low-dose Ag + ions could not only inhibit the inflammation process but also promote the bone healing by inducing healing-associated M2 polarization. Discussion: Using this surface modification strategy to modulate the macrophage-related immune response, rather than prevent the host response, maybe a promising strategy for implant surgeries in the future.

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“…Osteoblasts also secrete OPG, whose binding to RANKL, sequesters the latter, inhibiting osteoclastogenesis [ 34 , 35 ]. Together M-CSF and RANKL promote the survival and differentiation of osteoclast progenitors and consequently bone resorption [ 36 ]. Therefore, both the enhancement and the inhibition of the differentiation of osteoclasts and their progenitors are controlled by osteoblasts [ 37 ].…”

Section: Bone Structure and Metabolismmentioning

confidence: 99%

The Crossroads between Infection and Bone Loss

Oliveira

Gomes

2020

Microorganisms

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Bone homeostasis, based on a tight balance between bone formation and bone degradation, is affected by infection. On one hand, some invading pathogens are capable of directly colonizing the bone, leading to its destruction. On the other hand, immune mediators produced in response to infection may dysregulate the deposition of mineral matrix by osteoblasts and/or the resorption of bone by osteoclasts. Therefore, bone loss pathologies may develop in response to infection, and their detection and treatment are challenging. Possible biomarkers of impaired bone metabolism during chronic infection need to be identified to improve the diagnosis and management of infection-associated osteopenia. Further understanding of the impact of infections on bone metabolism is imperative for the early detection, prevention, and/or reversion of bone loss. Here, we review the mechanisms responsible for bone loss as a direct and/or indirect consequence of infection.

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Molecular determinants for the polarization of macrophage and osteoclast

Cited by 67 publications

References 159 publications

Single-cell RNA landscape of intratumoral heterogeneity and immunosuppressive microenvironment in advanced osteosarcoma

Single-cell RNA landscape of intratumoral heterogeneity and immunosuppressive microenvironment in advanced osteosarcoma

<p>Improved Immunoregulation of Ultra-Low-Dose Silver Nanoparticle-Loaded TiO<sub>2</sub> Nanotubes via M2 Macrophage Polarization by Regulating GLUT1 and Autophagy</p>

The Crossroads between Infection and Bone Loss

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