An Optimized Method to Generate Human Active Osteoclasts From Peripheral Blood Monocytes

Abdallah, Dina; Jourdain, Marie‐Laure; Braux, Julien; Guillaume, Christine; Gangloff, Sophie C.; Jacquot, Jacky; Velard, Frédéric

doi:10.3389/fimmu.2018.00632

Cited by 36 publications

(26 citation statements)

References 43 publications

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“…6G). Because RANKL has the ability to stimulate OC formation (22,23), we hypothesized that the supernatants of RA FLS stimulated with cNETs would promote OC formation. To test this hypothesis, PB CD14 + monocytes isolated from healthy volunteers were incubated in the presence or absence of supernatants of FLS stimulated with either NETs or cNETs.…”

Section: Cnets Activate Fls and Macrophages And Lead To Oc Differentimentioning

confidence: 99%

Neutrophil-mediated carbamylation promotes articular damage in rheumatoid arthritis

et al. 2020

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Formation of autoantibodies to carbamylated proteins (anti-CarP) is considered detrimental in the prognosis of erosive rheumatoid arthritis (RA). The source of carbamylated antigens and the mechanisms by which anti-CarP antibodies promote bone erosion in RA remain unknown. Here, we find that neutrophil extracellular traps (NETs) externalize carbamylated proteins and that RA subjects develop autoantibodies against carbamylated NET (cNET) antigens that, in turn, correlate with levels of anti-CarP. Transgenic mice expressing the human RA shared epitope (HLADRB1* 04:01) immunized with cNETs develop antibodies to citrullinated and carbamylated proteins. Furthermore, anti–carbamylated histone antibodies correlate with radiographic bone erosion in RA subjects. Moreover, anti–carbamylated histone–immunoglobulin G immune complexes promote osteoclast differentiation and potentiate osteoclast-mediated matrix resorption. These results demonstrate that carbamylated proteins present in NETs enhance pathogenic immune responses and bone destruction, which may explain the association between anti-CarP and erosive arthritis in RA.

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Section: Cnets Activate Fls and Macrophages And Lead To Oc Differentimentioning

confidence: 99%

Neutrophil-mediated carbamylation promotes articular damage in rheumatoid arthritis

et al. 2020

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“…In in-vitro culture, under the influence of M-CSF and RANKL treatment, PBMCs differentiate to macrophage/pre-OCs, which is followed by cell fusion. Mature and functional OCs are characterized by the presence of multiple nuclei in a very large unified cell (multi-nucleated giant cells) which produce TRAP (TRAP stain positive) (Fig 2A and 2B) [38][39][40][41][42].…”

Section: Discussionmentioning

confidence: 99%

Hibernating bear serum hinders osteoclastogenesis in-vitro

et al. 2020

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Bears do not suffer from osteoporosis during hibernation, which is associated with long-term inactivity, lack of food intake, and cold exposure. However, the mechanisms involved in bone loss prevention have scarcely been elucidated in bears. We investigated the effect of serum from hibernating Japanese black bears (Ursus thibetanus japonicus) on differentiation of peripheral blood mononuclear cells (PBMCs) to osteoclasts (OCs). PBMCs collected from 3 bears were separately cultured with 10% serum of 4 active and 4 hibernating bears (each individual serum type was assessed separately by a bear PBMCs), and differentiation were induced by treatment with macrophage colony stimulating factor (M-CSF) and receptor activator of NF-kB ligand (RANKL). PBMCs that were cultured with the active bear serum containing medium (ABSM) differentiated to multi-nucleated OCs, and were positive for TRAP stain. However, cells supplemented with hibernating bear serum containing medium (HBSM) failed to form OCs, and showed significantly lower TRAP stain (p < 0.001). On the other hand, HBSM induced proliferation of adipose derived mesenchymal stem cells (ADSCs) similarly to ABSM (p > 0.05), indicating no difference on cell growth. It was revealed that osteoclastogenesis of PBMCs is hindered by HBSM, implying an underlying mechanism for the suppressed bone resorption during hibernation in bears. In addition, this study for the first time showed the formation of bears' OCs in-vitro.

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“…Osteoclasts are bone‐resorbing cells that positively function in skeletal‐related issues as well as the remodeling of adult bone, and they have a characteristic ability to reuptake bone tissues . A former study found that miR‐155‐deficient mice showed reduced bone destruction, attributed to reduced generation of osteoclasts .…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‐155 inhibition up‐regulates LEPR to inhibit osteoclast activation and bone resorption via activation of AMPK in alendronate‐treated osteoporotic mice

et al. 2019

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Osteoporosis is characterized by a progressive increase in bone fragility, leading to low bone mass and structural deterioration of bone tissue. is highly expressed in osteoporosis. Thus, the current study aimed to investigate the effect of miR-155 on the inhibition of osteoclast activation and bone resorption by targeting leptin receptor (LEPR) through the adenosine monophosphate activated protein kinase (AMPK) pathway in alendronate-treated osteoporotic mice. An osteoporosis mouse model was established to examine the bone tension and bone density and the expression of miR-155 in osteoclasts. Binding sites between miR-155 and LEPR were verified. Osteoclasts in the treatment group were transfected with different mimic, inhibitor, vector, or siRNA for subsequent experiments. The expression of miR-155, LEPR, AMPK, p-AMPK, RANKL, OPG, M-CSF, RANK, TRAP, Bax, Bcl-2, and the contents of TNF-α and IL-1β were all examined. The proliferation and bone resorption of osteoclasts were also detected. Mice with osteoporosis exhibited decreased bone density and bone tension, along with elevated expression of miR-155. LEPR was verified as a target gene of miR-155. Down-regulated miR-155 was found to increase the expression of LEPR, AMPK, p-AMPK, OPG, Bax, decrease expression of TNF-α, IL-1β, RANKL, M-CSF, RANK, TRAP, Bcl-2, inhibit the cell proliferation and bone resorption of osteoclasts. Taken together, decreased miR-155 up-regulated LEPR via activation of AMPK, which ultimately repressed osteoclast activation and bone resorption of osteoclasts in alendronatetreated osteoporotic mice. K E Y W O R D S AMPK pathway, bone resorption, LEPR, microRNA-155, osteoclast, osteoporosis, proliferationAbbreviations: AMPK, adenosine monophosphate activated protein kinase; ANOVA, analysis of variance; ECL, electrochemiluminescence; ELISA, enzyme-linked immunosorbent assay; FBS, fetal bovine serum; LEPR, leptin receptor; M-CSF, macrophage colony stimulating factor; miR-155, microRNA-155; NC, negative control; OD, optical density; PCV, pack cell volume; RT-qPCR, reverse transcription quantitative polymerase chain reaction; SDS-PAGE, sodium dodecyl sulfate polyacrylamide gel electrophoresis; TBST, tris buffered saline tween; TRAP, tartaric acid phosphatase; TRAP, tartrate resistant acid phosphatase; WT, wild type.

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An Optimized Method to Generate Human Active Osteoclasts From Peripheral Blood Monocytes

Cited by 36 publications

References 43 publications

Neutrophil-mediated carbamylation promotes articular damage in rheumatoid arthritis

Neutrophil-mediated carbamylation promotes articular damage in rheumatoid arthritis

Hibernating bear serum hinders osteoclastogenesis in-vitro

MicroRNA‐155 inhibition up‐regulates LEPR to inhibit osteoclast activation and bone resorption via activation of AMPK in alendronate‐treated osteoporotic mice

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