scholarly journals Oxygen-derived free radicals stimulate osteoclastic bone resorption in rodent bone in vitro and in vivo.

1990 ◽  
Vol 85 (3) ◽  
pp. 632-639 ◽  
Author(s):  
I R Garrett ◽  
B F Boyce ◽  
R O Oreffo ◽  
L Bonewald ◽  
J Poser ◽  
...  
Keyword(s):  
Free Radicals ◽  
Bone Resorption ◽  
Osteoclastic Bone Resorption ◽  
Oxygen Derived Free Radicals

Tri-iodothyronine stimulates rat osteoclastic bone resorption by an indirect effect

1992 ◽  
Vol 133 (3) ◽  
pp. 327-331 ◽  
Author(s):  
T. J. Allain ◽  
T. J. Chambers ◽  
A. M. Flanagan ◽  
A. M. McGregor
Keyword(s):  
Bone Resorption ◽  
Bone Cells ◽  
Direct Action ◽  
Fold Increase ◽  
Osteoclastic Bone Resorption ◽  
Neonatal Rat ◽  
Long Bones ◽  
Umr 106

ABSTRACT Tri-iodothyronine (T3) increases bone resorption in vivo and in vitro. In order to understand further the mechanisms by which this occurs we studied the effects of T3 at concentrations in the range of 1 pmol/l–1 μmol/l on bone resorption by osteoclasts isolated from neonatal rat long bones. Osteoclasts were disaggregated and incubated either with or without UMR 106 cells or with mixed bone cells. We found that there was no effect of T3 on bone resorption by osteoclasts incubated alone or co-cultured with UMR 106 cells. However, in culture with mixed bone cells there was a significant relationship between the concentration of T3 and bone resorption (r = 0·54, P= 0·01) The greatest effect was observed at a T3 concentration of 1 μmol/l at which a 1·8-fold increase in resorption was seen compared with control (P <0·005; paired t-test). We conclude that the ability of T3 to increase osteoclastic bone resorption is not due to a direct action of T3 on osteoclasts but is mediated by another cell present in bone. The observation that UMR 106 cells are unable to mediate this effect suggests that either the mediating cell is not osteoblastic or the phenotype of UMR 106 does not conform to the phenotype of osteoblastic cells that mediate the T3 responsiveness of bone. Journal of Endocrinology (1992) 133, 327–331

Leukotriene B4 stimulates osteoclastic bone resorption both in vitro and in vivo

2009 ◽  
Vol 11 (11) ◽  
pp. 1619-1627 ◽  
Author(s):  
Carlos Garcia ◽  
Brendan F. Boyce ◽  
James Gilles ◽  
Mark Dallas ◽  
Mei Qiao ◽  
...  
Keyword(s):  
Bone Resorption ◽  
Leukotriene B4 ◽  
Osteoclastic Bone Resorption

Gambogic acid inhibits osteoclast formation and ovariectomy-induced osteoporosis by suppressing the JNK, p38 and Akt signalling pathways

2015 ◽  
Vol 469 (3) ◽  
pp. 399-408 ◽  
Author(s):  
Jianjun Ma ◽  
Yan Ma ◽  
Xuqiang Liu ◽  
Shuai Chen ◽  
Chao Liu ◽  
...  
Keyword(s):  
Bone Resorption ◽  
Natural Compound ◽  
Osteoclast Formation ◽  
Osteoclastic Bone Resorption ◽  
Signalling Pathways ◽  
Gambogic Acid

we report that the natural compound gambogic acid (GBA) inhibits osteoclast formation, thereby attenuating osteoclastic bone resorption in vitro and in vivo. Furthermore, we found that GBA acted by suppressing activation of JNK, p38 and Akt signalling.

Chalcone T4, a novel chalconic compound, inhibits inflammatory bone resorption in vivo and suppresses osteoclastogenesis in vitro

2021 ◽  
Author(s):  
Natalie Aparecida Rodrigues Fernandes ◽  
Angelo Constantino Camilli ◽  
Laura Andrea Gonzalez Maldonado ◽  
Cindy Grace Pérez Pacheco ◽  
Amanda Favoreto Silva ◽  
...  
Keyword(s):  
Bone Resorption

scholarly journals Biological Effects of β-Glucans on Osteoclastogenesis

Molecules ◽  
2021 ◽  
Vol 26 (7) ◽  
pp. 1982
Author(s):  
Wataru Ariyoshi ◽  
Shiika Hara ◽  
Ayaka Koga ◽  
Yoshie Nagai-Yoshioka ◽  
Ryota Yamasaki
Keyword(s):  
Bone Resorption ◽  
Bone Marrow Cells ◽  
Biological Effects ◽  
Osteoclast Differentiation ◽  
Treatment Strategies ◽  
Alcaligenes Faecalis ◽  
Osteoclast Formation ◽  
Osteoclast Precursors

Although the anti-tumor and anti-infective properties of β-glucans have been well-discussed, their role in bone metabolism has not been reviewed so far. This review discusses the biological effects of β-glucans on bone metabolisms, especially on bone-resorbing osteoclasts, which are differentiated from hematopoietic precursors. Multiple immunoreceptors that can recognize β-glucans were reported to be expressed in osteoclast precursors. Coordinated co-stimulatory signals mediated by these immunoreceptors are important for the regulation of osteoclastogenesis and bone remodeling. Curdlan from the bacterium Alcaligenes faecalis negatively regulates osteoclast differentiation in vitro by affecting both the osteoclast precursors and osteoclast-supporting cells. We also showed that laminarin, lichenan, and glucan from baker’s yeast, as well as β-1,3-glucan from Euglema gracilisas, inhibit the osteoclast formation in bone marrow cells. Consistent with these findings, systemic and local administration of β-glucan derived from Aureobasidium pullulans and Saccharomyces cerevisiae suppressed bone resorption in vivo. However, zymosan derived from S. cerevisiae stimulated the bone resorption activity and is widely used to induce arthritis in animal models. Additional research concerning the relationship between the molecular structure of β-glucan and its effect on osteoclastic bone resorption will be beneficial for the development of novel treatment strategies for bone-related diseases.

scholarly journals Estrogen Decreases Cytoskeletal Organization by Forming an ERα/SHP2/c-Src Complex in Osteoclasts to Protect against Ovariectomy-Induced Bone Loss in Mice

Antioxidants ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 619
Author(s):  
Hyun-Jung Park ◽  
Malihatosadat Gholam-Zadeh ◽  
Sun-Young Yoon ◽  
Jae-Hee Suh ◽  
Hye-Seon Choi
Keyword(s):  
Bone Resorption ◽  
Bone Loss ◽  
Ring Formation ◽  
Tartrate Resistant Acid Phosphatase ◽  
Actin Ring ◽  
Collagen Crosslinks ◽  
Trap Staining ◽  
Src Activation

Loss of ovarian function is closely related to estrogen (E2) deficiency, which is responsible for increased osteoclast (OC) differentiation and activity. We aimed to investigate the action mechanism of E2 to decrease bone resorption in OCs to protect from ovariectomy (OVX)-induced bone loss in mice. In vivo, tartrate-resistant acid phosphatase (TRAP) staining in femur and serum carboxy-terminal collagen crosslinks-1 (CTX-1) were analyzed upon E2 injection after OVX in mice. In vitro, OCs were analyzed by TRAP staining, actin ring formation, carboxymethylation, determination of reactive oxygen species (ROS) level, and immunoprecipitation coupled with Western blot. In vivo and in vitro, E2 decreased OC size more dramatically than OC number and Methyl-piperidino-pyrazole hydrate dihydrochloride (MPPD), an estrogen receptor alpha (ERα) antagonist, augmented the OC size. ERα was found in plasma membranes and E2/ERα signaling affected receptor activator of nuclear factor κB ligand (RANKL)-induced actin ring formation by rapidly decreasing a proto-oncogene tyrosine-protein kinase, cellular sarcoma (c-Src) (Y416) phosphorylation in OCs. E2 exposure decreased physical interactions between NADPH oxidase 1 (NOX1) and the oxidized form of c-Src homology 2 (SH2)-containing protein tyrosine phosphatase 2 (SHP2), leading to higher levels of reduced SHP2. ERα formed a complex with the reduced form of SHP2 and c-Src to decrease c-Src activation upon E2 exposure, which blocked a signal for actin ring formation by decreased Vav guanine nucleotide exchange factor 3 (Vav3) (p–Y) and Ras-related C3 botulinum toxin substrate 1 (Rac1) (GTP) activation in OCs. E2/ERα signals consistently inhibited bone resorption in vitro. In conclusion, our study suggests that E2-binding to ERα forms a complex with SHP2/c-Src to attenuate c-Src activation that was induced upon RANKL stimulation in a non-genomic manner, resulting in an impaired actin ring formation and reducing bone resorption.

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