scholarly journals The effect of bisphosphonate treatment on osteoclast precursor cells in postmenopausal osteoporosis: The TRIO study

Bone ◽  
2016 ◽  
Vol 92 ◽  
pp. 94-99 ◽  
Author(s):  
F. Gossiel ◽  
C. Hoyle ◽  
E.V. McCloskey ◽  
K.E. Naylor ◽  
J. Walsh ◽  
...  
Keyword(s):  
Postmenopausal Osteoporosis ◽  
Precursor Cells ◽  
Osteoclast Precursor ◽  
Bisphosphonate Treatment

The effect of bisphosphonate treatment on osteoclast precursor cells in postmenopausal women with rsteoporosis: The TRIO study

2014 ◽  
Author(s):  
Fatma Gossiel ◽  
Christopher Hoyle ◽  
Eugene McCloskey ◽  
Jennifer Walsh ◽  
Nicola Peel ◽  
...  
Keyword(s):  
Postmenopausal Women ◽  
Precursor Cells ◽  
Osteoclast Precursor ◽  
Bisphosphonate Treatment

scholarly journals The effect of denosumab treatment on osteoclast precursor cells in postmenopausal osteoporosis

Bone Reports ◽  
2020 ◽  
Vol 13 ◽  
pp. 100457
Author(s):  
Andreas Fontalis ◽  
Fatma Gossiel ◽  
Marian Schini ◽  
Jennifer Walsh ◽  
Richard Eastell
Keyword(s):  
Postmenopausal Osteoporosis ◽  
Precursor Cells ◽  
Osteoclast Precursor ◽  
Denosumab Treatment

The effect of bisphosphonate treatment on sclerostin levels in postmenopausal osteoporosis: the TRIO study

2014 ◽  
Author(s):  
Fatma Gossiel ◽  
Kim Naylor ◽  
Eugene McCloskey ◽  
Nicola Peel ◽  
Jennifer Walsh ◽  
...  
Keyword(s):  
Postmenopausal Osteoporosis ◽  
Bisphosphonate Treatment

An adherent condition is required for formation of multinuclear osteoclasts in the presence of macrophage colony-stimulating factor and receptor activator of nuclear factor κB ligand

Blood ◽  
2000 ◽  
Vol 96 (13) ◽  
pp. 4335-4343 ◽  
Author(s):  
Takeshi Miyamoto ◽  
Fumio Arai ◽  
Osamu Ohneda ◽  
Katsumasa Takagi ◽  
Dirk M. Anderson ◽  
...  
Keyword(s):  
Culture Medium ◽  
Osteoclast Differentiation ◽  
Nuclear Factor Κb ◽  
Precursor Cells ◽  
Osteoclast Precursor ◽  
Nuclear Factor ◽  
Receptor Activator ◽  
Multinuclear Cells ◽  
Differentiation And Proliferation

Abstract Identification of receptor activator of nuclear factor-κB (RANK) and RANK-ligand (RANKL) has provided new insights into the osteoclast differentiation pathway. Osteoclast precursor cells were isolated using monoclonal antibodies against c-Fms and RANK, and the effect of adherence on the in vitro differentiation and proliferation of these cells was examined in 2 different types of stromal-cell–free culture systems: a semisolid culture medium (a nonadherent system) and a liquid culture medium (an adherent system). Osteoclast precursor cells were not able to differentiate into mature osteoclasts efficiently in the semisolid culture system. Trimerized RANKL enhanced osteoclast differentiation in semisolid cultures, but not to the extent seen when cells were allowed to adhere to plastic. Initial precursor cells were capable of differentiating into macrophages or osteoclasts. Once these cells were transferred to adherent conditions, striking differentiation was induced. Multinuclear cells were observed even after they had displayed phagocytic activity, which suggests that cell adhesion plays an important role in the differentiation of osteoclast precursor cells. Integrins, especially the arginine-glycine-aspartic acid (RGD)–recognizing integrins αv and β3, were needed for osteoclast-committed precursor cells to proliferate in order to form multinuclear osteoclasts, and the increase in cell density affected the formation of multinuclear cells. A model of osteoclast differentiation with 2 stages of precursor development is proposed: (1) a first stage, in which precursor cells are bipotential and capable of anchorage-independent growth, and (2) a second stage, in which the further proliferation and differentiation of osteoclast-committed precursor cells is anchorage-dependent.

scholarly journals Analysis of TNFR2-mediated functions on osteoclast precursor cells

2010 ◽  
Vol 69 (Suppl 2) ◽  
pp. A35-A36 ◽  
Author(s):  
S. Bluml ◽  
N. Binder ◽  
B. Niederreiter ◽  
G. Superti-Furga ◽  
J. Smolen ◽  
...  
Keyword(s):  
Precursor Cells ◽  
Osteoclast Precursor

scholarly journals Decoy Receptor 3 Promotes Preosteoclast Cell Death via Reactive Oxygen Species-Induced Fas Ligand Expression and the IL-1α/IL-1 Receptor Antagonist Pathway

2020 ◽  
Vol 2020 ◽  
pp. 1-11
Author(s):  
Yi-Jen Peng ◽  
Ching-Tsung Peng ◽  
Yi-Hsuan Lin ◽  
Gu-Jiun Lin ◽  
Shing-Hwa Huang ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Bone Resorption ◽  
Fas Ligand ◽  
Interleukin 1 ◽  
Reactive Oxygen ◽  
Precursor Cells ◽  
Osteoclast Precursor ◽  
Oxygen Species ◽  
Decoy Receptor ◽  
Decoy Receptor 3

Purpose. Interleukin-1α (IL-1α) is a potent cytokine that plays a role in inflammatory arthritis and bone loss. Decoy receptor 3 (DCR3) is an immune modulator of monocytes and macrophages. The aim of this study was to investigate the mechanism of DCR3 in IL-1α-induced osteoclastogenesis. Methods. We treated murine macrophages with DCR3 during receptor activator of nuclear factor kappa Β ligand- (RANKL-) plus IL-1α-induced osteoclastogenesis to monitor osteoclast formation by tartrate-resistant acid phosphatase (TRAP) staining. Osteoclast activity was assessed using a pit formation assay. The mechanisms of inhibition were studied by biochemical analyses, including RT-PCR, immunofluorescent staining, flow cytometry, an apoptosis assay, immunoblotting, and ELISA. Results. DCR3 suppresses IL-1α-induced osteoclastogenesis in both primary murine bone marrow-derived macrophages (BMM) and RAW264.7 cells as it inhibits bone resorption. DCR3 induces RANKL-treated osteoclast precursor cells to express IL-1α, secretory IL-1ra (sIL-1ra), intracellular IL-1ra (icIL-1ra), reactive oxygen species (ROS), and Fas ligand and to activate IL-1α-induced interleukin-1 receptor-associated kinase 4 (IRAK4). The suppression of DCR3 during RANKL- or IL-1α-induced osteoclastogenesis may be due to the abundant secretion of IL-1ra, accumulation of ROS, and expression of Fas ligand in apoptotic osteoclast precursor cells. Conclusions. We concluded that there is an inhibitory effect of DCR3 on osteoclastogenesis via ROS accumulation and ROS-induced Fas ligand, IL-1α, and IL-1ra expression. Our results suggested that the upregulation of DCR3 in preosteoclasts might be a therapeutic target in inflammatory IL-1α-induced bone resorption.

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