Primary human bone marrow adipocytes support TNF-α-induced osteoclast differentiation and function through RANKL expression

Goto, Hisataka; Hozumi, Akira; Osaki, Makoto; Fukushima, Tatsuya; Sakamoto, Kazutaka; Yonekura, Akihiko; Tomita, Masato; Furukawa, Koichi; Shindo, Hiroyuki; Baba, Hideo

doi:10.1016/j.cyto.2011.09.005

Cited by 72 publications

(56 citation statements)

References 34 publications

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“…However, both OPG and RANKL, and OPG in particular, are regulated not only by 17β-estradiol, but also by other hormones and cytokines (maybe also pro-inflammatory cytokines), whose effect might be similar or opposite to that of 17β-estradiol [27]. It has been demonstrated that pro-inflammatory cytokines influence the bone tissue directly and/or indirectly, via the RANKL/RANK/OPG system [27][28][29][30][31][32][33][34][35][36][37][38][39]. Since it has been documented that IL-1β, IL-6, and TNF-α stimulate bone resorption both in vitro and in vivo [27][28][29][30], it seems reasonable to presume that any potential disturbances in the production of these cytokines in patients with AN might play a role in the development of osteoporosis.…”

Section: Discussionmentioning

confidence: 99%

“…TNF-α enhances RANKL expression and bone resorption by osteoclasts [36][37][38][39]. The above data suggest that cytokines may regulate osteoclastogenesis not only directly, but also indirectly via the RANKL/ /RANK/OPG system [27][28][29][30][31][32][33][34][35][36][37][38][39].…”

Section: Prace Oryginalnementioning

confidence: 99%

“…The above data suggest that cytokines may regulate osteoclastogenesis not only directly, but also indirectly via the RANKL/ /RANK/OPG system [27][28][29][30][31][32][33][34][35][36][37][38][39]. Through an increase in the expression of RANKL and/or a decrease in OPG expression, IL-1β, IL-6, or TNF-α may suppress the OPG/RANKL ratio resulting in enhanced bone resorption [27][28][29][30][31][32][33][34][35][36][37][38][39].…”

Section: Prace Oryginalnementioning

confidence: 99%

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Wybrane cytokiny prozapalne, metabolizm kostny, osteoprotegeryna i ligand receptora aktywatora czynnika jądrowego-kB u dziewcząt z jadłowstrętem psychicznym

Ostrowska

Ziora

Oświęcimska

et al. 2015

Endokrynologia Polska

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Section: Discussionmentioning

confidence: 99%

Section: Prace Oryginalnementioning

confidence: 99%

Section: Prace Oryginalnementioning

confidence: 99%

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Wybrane cytokiny prozapalne, metabolizm kostny, osteoprotegeryna i ligand receptora aktywatora czynnika jądrowego-kB u dziewcząt z jadłowstrętem psychicznym

Ostrowska

Ziora

Oświęcimska

et al. 2015

Endokrynologia Polska

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“…Recent data points to the involvement of adipocytes in osteoclast differentiation and function [24]. Promotion of osteoclastogenesis by adipocytes could explain an increased adipocyte component of bone marrow in osteoporosis, leading to bone resorption eventually.…”

Section: Discussionmentioning

confidence: 99%

“…In such circumstances there is no demand for ectopic bones to generate new osteoblasts or remodeling, and the stromal cells in their marrow switch their differentiation into adipocytes, instead of into osteoblasts. Adipocytes, in turn, promote osteoclastic differentiation, thus accelerating degradation of ectopic and aging bones [24,28].…”

Section: Discussionmentioning

confidence: 99%

The adipocyte component of bone marrow in heterotopic bone induced by demineralized incisor grafts

Włodarski¹,

Galus²,

Brodzikowska³

et al. 2012

Folia Histochem Cytobiol.

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Abstract:The relative proportion of adipocytes to hematopoietic elements in the marrow of heterotopically induced bone evaluated 4-42 weeks post implantation of demineralized murine incisors was estimated by histological analysis of hematoxylin-eosin stained tissue sections. Using computerized image analysis of microphotographs, the proportion of nuclear cells vs. adipocytes was ascertained. The percentage of adipocytes in marrow increases over time. Such an effect, the replacement of myelopoietic marrow by adipogenic (yellow) marrow and the resorption of induced bone, is observed in human osteoporosis. A decline in the non-adipogenic cell compartments of bone marrow accompanying induced bone begins in the fourth week of induction, gradually progresses until the 26 th week, and does not change after that. The luminosity, a parameter used in image analysis and proportional to the number of nuclear cells, was 124 ± 3 in hematopoietic femoral bone marrow, and that of bone marrow of the induced bone was of a similar value (117 ± 8) in the fourth week. An evident decline in luminosity of bone marrow filling the foci of heterotopic bone was observed in samples taken at nine weeks (82 ± 20). This process progressed until the 26 th week, reaching a luminosity of 70 ± 21. At the 42 nd week, the luminosity remained at the same level (71 ± 27). This indicates that the replacement of hematopoietic bone marrow of heterotopically induced bone by unilocular adipocytes begins relatively early (the fourth week) and is persistent.

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Bmi‐1 Epigenetically Orchestrates Osteogenic and Adipogenic Differentiation of Bone Marrow Mesenchymal Stem Cells to Delay Bone Aging

Zhao,

Chen,

Wang

et al. 2024

Advanced Science

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With the increase in the aging population, senile osteoporosis (SOP) has become a major global public health concern. Here, it is found that Prx1 and Bmi‐1 co‐localized in trabecular bone, bone marrow cavity, endosteum, and periosteum. Prx1‐driven Bmi‐1 knockout in bone‐marrow mesenchymal stem cells (BMSCs) reduced bone mass and increased bone marrow adiposity by inhibiting osteoblastic bone formation, promoting osteoclastic bone resorption, downregulating the proliferation and osteogenic differentiation of BMSCs, and upregulating the adipogenic differentiation of BMSCs. However, Prx1‐driven Bmi‐1 overexpression showed a contrasting phenotype to Prx1‐driven Bmi‐1 knockout in BMSCs. Regarding mechanism, Bmi‐1‐RING1B bound to DNMT3A and promoted its ubiquitination and inhibited DNA methylation of Runx2 at the region from 45047012 to 45047313 bp, thus promoting the osteogenic differentiation of BMSCs. Moreover, Bmi‐1‐EZH2 repressed the transcription of Cebpa by promoting H3K27 trimethylation at the promoter region −1605 to −1596 bp, thus inhibiting the adipogenic differentiation of BMSCs. It is also found that Prx1‐driven Bmi‐1 overexpression rescued the SOP induced by Prx1‐driven Bmi‐1 knockout in BMSCs. Thus, Bmi‐1 functioned as a hub protein in the epigenetic regulation of BMSCs differentiation to delay bone aging. The Prx1‐driven Bmi‐1 overexpression in BMSCs can be used as an approach for the translational therapy of SOP.

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Primary human bone marrow adipocytes support TNF-α-induced osteoclast differentiation and function through RANKL expression

Cited by 72 publications

References 34 publications

Wybrane cytokiny prozapalne, metabolizm kostny, osteoprotegeryna i ligand receptora aktywatora czynnika jądrowego-kB u dziewcząt z jadłowstrętem psychicznym

Wybrane cytokiny prozapalne, metabolizm kostny, osteoprotegeryna i ligand receptora aktywatora czynnika jądrowego-kB u dziewcząt z jadłowstrętem psychicznym

The adipocyte component of bone marrow in heterotopic bone induced by demineralized incisor grafts

Bmi‐1 Epigenetically Orchestrates Osteogenic and Adipogenic Differentiation of Bone Marrow Mesenchymal Stem Cells to Delay Bone Aging

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