C/EBPβ Mediates Osteoclast Recruitment by Regulating Endothelial Progenitor Cell Expression of SDF-1α

Fu, Sheng-Long; Pang, Haijun; Xu, Jiake; Wu, Xiang

doi:10.1371/journal.pone.0091217

Cited by 9 publications

(13 citation statements)

References 51 publications

(63 reference statements)

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“…Other groups have previously shown the ability of S1P/S1PR agonism to promote the motility/migration of RAW264.7 cells, therefore, we set out to validate these findings using S1P (S1PR agonist), SEW2871 (S1PR1 agonist) and known monocyte chemotactic factor SDF-1α prior to performing our own studies (35). Indeed, we also demonstrate robust dose-dependent enhancement of RAW264.7 cell transwell migration with all three agents and thereby validated published data (Fig.…”

Section: Resultsmentioning

confidence: 82%

TGFβ-Mediated induction of SphK1 as a potential determinant in human MDA-MB-231 breast cancer cell bone metastasis

et al. 2015

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Mechanistic understanding of the preferential homing of circulating tumor cells to bone and their perturbation on bone metabolism within the tumor-bone microenvironment remains poorly understood. Alterations in both TGFβ signaling and sphingolipid metabolism results in the promotion of tumor growth and metastasis. Previous studies using MDA-MB-231 human breast cancer-derived cell lines of variable metastatic potential were queried for changes in sphingolipid metabolism genes to explore correlations between TGFβ-dependence and bone metastatic behavior. Of these genes, only sphingosine kinase-1 (SPHK1) was identified to be significantly increased following TGFβ treatment. Induction of SPHK1 expression correlated to the degree of metastatic capacity in these MDA-MB-231-derived cell lines. We demonstrate that TGFβ mediates the regulation of SPHK1 gene expression, protein kinase activity and is critical to MDA-MB-231 cell viability. Furthermore, a bioinformatic analysis of human breast cancer gene expression supports SPHK1 as a hallmark TGFβ target gene that also bears the genetic fingerprint of the basal-like/triple-negative breast cancer molecular subtype. This data suggests a potential new signaling axis between TGFβ/SphK1 that may play a role in the development, prognosis or the clinical phenotype associated with tumor-bone metastasis.

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Section: Resultsmentioning

confidence: 82%

TGFβ-Mediated induction of SphK1 as a potential determinant in human MDA-MB-231 breast cancer cell bone metastasis

et al. 2015

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“…Evidences have shown that EPCs can secrete SDF‐1. Additionally, Fu, Pang, Xu, & Wu, observed that EPCs promote survival, migration, and differentiation of osteoclast precursors by producing VEGF A, SDF‐1, and transforming growth factor β1 (TGF‐β1) (Fu et al, ; Pang et al, ), which supports the role of SDF‐1 in the crosstalk between EPCs and osteoclasts. Meanwhile, it has been reported that irradiation elevated another chemokine CX3CL1 by vascular endothelium and stimulated osteoclastogenesis (Han et al, ).…”

Section: Discussionmentioning

confidence: 89%

Suppressing angiogenesis regulates the irradiation‐induced stimulation on osteoclastogenesis in vitro

Tong

Zhu

Wang

et al. 2017

Journal Cellular Physiology

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Ionizing radiation-induced bone loss is a potential health concern in radiotherapy, occupational exposure, and astronauts. Although impaired bone vasculature and reduced proliferation of bone-forming osteoblasts has been implicated in this process, it has not been clearly characterized that whether radiation affects the growth of bone-resorbing osteoclasts. The molecular crosstalk between different cell populations in the skeletal system has not yet been elucidated in detail, especially between the increased bone resorption at early stage of post-irradiation and bone marrow-derived endothelial progenitor cells (BM-EPCs). In order to further understand the mechanisms involved in radiation-induced bone loss at the cellular level, we assessed the effects of irradiation on angiogenesis of BM-EPCs and osteoclastogenesis of receptor activator for nuclear factor-κB ligand (RANKL)-stimulated RAW 264.7 cells and crosstalk between these cell populations. We herein found significantly dysfunction of BM-EPCs in response to irradiation at a dose of 2 Gy, including inhibited proliferation, migration, tube-forming abilities, and downregulated expression of pro-angiogenesis vascular endothelial growth factors A (VEGF A). Meanwhile, we observed that irradiation promoted osteoclastogenesis of RANKL-stimulated RAW 264.7 cells directly or indirectly. These results provide quantitative evidences of irradiation induced osteoclastogenesis at a cellular level, and strongly suggest the involvement of osteoclastogenesis, angiogenesis and crosstalk between bone marrow cells in the radiation-induced bone loss. This study may provide new insights for the early diagnosis and intervention of bone loss post-irradiation.

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“…They have also been reported to enhance osteogenic differentiation capacities of osteoblast precursors in vitro and in vivo [17,30]. With regard to the role of EPCs in osteoclast formation and function, previous reports have shown that EPCs support the survival, migration, and differentiation of RAW 264.7 cells, a model of osteoclastic monocyte precursors [19,20]. In this study, we found that EPCs derived from mouse umbilical cord blood promoted the proliferation, migration and osteoclastic differentiation of primary mouse BMMs in a EPC-BMM coculture system.…”

Section: Discussionmentioning

confidence: 98%

“…Emerging evidence suggests that EPCs may also play a role in osteoclast formation and function. Specifically, EPCs have been reported to support the survival, migration, and differentiation of RAW 264.7 cells, a model of osteoclastic monocyte precursors, through multiple signaling pathways [19,20]. However, whether EPCs can influence osteoclastogenesis by bone marrow-derived macrophages (BMMs) is not clear.…”

Section: Introductionmentioning

confidence: 99%

Endothelial Progenitor Cells Enhance the Migration and Osteoclastic Differentiation of Bone Marrow-Derived Macrophages in vitro and in a Mouse Femur Fracture Model through Talin-1

Cui

Hou

et al. 2018

Cell Physiol Biochem

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Background/Aims: Bone resorption mediated by osteoclasts plays an important role in bone healing. Endothelial progenitor cells (EPCs) promote bone repair by stimulating neovascularization and osteogenesis. However, the role of EPCs in osteoclast formation and function is not well defined. The aim of this study was to elucidate mechanisms of EPCs in osteoclast formation and function. Methods: In this study, we examined the effects of EPCs on the proliferation, migration and osteoclastic differentiation of primary mouse bone marrow-derived macrophages (BMMs) in a co-culture system in vitro. We also evaluated the effects of EPC co-transplantation on the homing and osteoclastic differentiation of transplanted BMMs in a mouse bone fracture model in vivo. The technology of immunofluorescence, immunohistochemical, western blot, Rt-PCR, cell co-culture and Transwell were used in this study. Results: EPCs secreted TGF-β1 in the EPC-BMM co-culture medium and increased Talin-1 expression in the co-cultured BMMs. Treatment with a TGF-β1 neutralizing antibody or Talin-1 silencing in BMMs completely inhibited BMM osteoclastic differentiation in the co-culture system. These results indicated that the osteoclastogenic effects of EPCs were mediated by TGF-β1-mediated Talin-1 expression in BMMs. In the femur fracture model, BMMs co-transplanted with EPCs exhibited enhanced engraftment into the fracture site and osteoclastic differentiation compared with those transplanted alone. Mice treated with EPC-BMM co-transplantation exhibited increased neovascularization at the fracture site and accelerated fracture healing compared with those treated with BMMs alone. Conclusion: Taken together, the results suggest that EPCs can promote bone repair by enhancing recruitment and differentiation of osteoclast precursors.

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C/EBPβ Mediates Osteoclast Recruitment by Regulating Endothelial Progenitor Cell Expression of SDF-1α

Cited by 9 publications

References 51 publications

TGFβ-Mediated induction of SphK1 as a potential determinant in human MDA-MB-231 breast cancer cell bone metastasis

TGFβ-Mediated induction of SphK1 as a potential determinant in human MDA-MB-231 breast cancer cell bone metastasis

Suppressing angiogenesis regulates the irradiation‐induced stimulation on osteoclastogenesis in vitro

Endothelial Progenitor Cells Enhance the Migration and Osteoclastic Differentiation of Bone Marrow-Derived Macrophages in vitro and in a Mouse Femur Fracture Model through Talin-1

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