The inhibitory effects of Citrus unshiu Markovich extracts on the receptor activator of nuclear factor-kappa-B ligand-mediated osteoclast differentiation and function

2015 ◽  
Vol 24 (5) ◽  
pp. 1837-1843 ◽  
Author(s):  
Jong Min Baek ◽  
Jung-Youl Min ◽  
Ju-Young Kim ◽  
Kwon-Ha Yoon ◽  
Min Kyu Choi ◽  
...  
Keyword(s):  
Nuclear Factor Kappa B ◽  
Osteoclast Differentiation ◽  
Citrus Unshiu ◽  
Nuclear Factor ◽  
Inhibitory Effects ◽  
Nuclear Factor Kappa ◽  
Receptor Activator ◽  
And Function

scholarly journals Osteoclast differentiation antigen, distinct from receptor activator of nuclear factor kappa B, is involved in osteoclastogenesis under calcitonin-regulated conditions

2001 ◽  
Vol 170 (1) ◽  
pp. 175-183 ◽  
Author(s):  
T Kukita ◽  
A Kukita ◽  
T Watanabe ◽  
T Iijima
Keyword(s):  
Cell Surface ◽  
Nuclear Factor Kappa B ◽  
Osteoclast Differentiation ◽  
Cell Formation ◽  
Nuclear Factor ◽  
Metabolic Bone Diseases ◽  
Escape Phenomenon ◽  
Nuclear Factor Kappa ◽  
Receptor Activator ◽  
Nf Kappab

Although calcitonin has been clinically utilized as a primary treatment for several metabolic bone diseases, its inhibitory effects against osteoclastic function diminish after several days owing to the calcitonin 'escape phenomenon'. We have previously found a unique cell-surface antigen (Kat1-antigen) expressed on rat osteoclasts. Here we show evidence that, in the presence of calcitonin, the Kat1-antigen is involved in osteoclastogenesis. Treatment of bone marrow cultures for forming osteoclast-like cells with anti-Kat1-antigen monoclonal antibody (mAb Kat1) provoked a marked stimulation of osteoclast-like cell formation only in the presence of calcitonin but not in its absence. Osteoclastogenesis stimulated by the receptor activator of nuclear factor kappa B (NF-kappaB) ligand/osteoclast differentiation factor was further augmented by mAb Kat1 in the presence of calcitonin. Furthermore, even in the presence of the osteoprotegerin/osteoclast inhibitory factor, mAb Kat1 induced osteoclast-like cell formation. Our current data suggest that the Kat1-antigen is a molecule that is distinct from receptor activator of NF-kappaB. The presence of the unique Kat1-antigen on cells in the osteoclast lineage appears to contribute to the fine regulation of osteoclastogenesis in vivo. Expression of this cell-surface molecule in cells in the osteoclast lineage may partly explain the mechanism responsible for the escape phenomenon.

scholarly journals Triiodothyronine (T3) does not induce Rankl expression in rat Ros 17/2.8 cells

2008 ◽  
Vol 52 (1) ◽  
pp. 109-113 ◽  
Author(s):  
Patrícia P. Saraiva ◽  
Silvania S. Teixeira ◽  
Célia Regina Nogueira ◽  
Carlos Roberto Padovani
Keyword(s):  
Messenger Rna ◽  
Nuclear Factor Kappa B ◽  
Osteoclast Differentiation ◽  
Hormone Treatment ◽  
Nuclear Factor ◽  
Rankl Expression ◽  
Loss Mechanism ◽  
Nuclear Factor Kappa ◽  
Rankl Mrna ◽  
Receptor Activator

Osteoclastogenesis may be regulated via activation of the RANK/RANKL (receptor activator of nuclear factor-kappa B/ receptor activator of nuclear factor-kappa B ligand) system, which is mediated by osteoblasts. However, the bone loss mechanism induced by T3 (triiodothyronine) is still controversial. In this study, osteoblastic lineage rat cells (ROS 17/2.8) were treated with T3 (10-8 M, 10-9 M, and 10-10 M), and RANKL mRNA (messenger RNA) expression was measured by semiquantitative RT-PCR. Our results show that T3 concentrations used did not significantly enhance RANKL expression compared to controls without hormone treatment. This data suggests that other mechanisms, unrelated to the RANK/RANKL system, might be to activate osteoclast differentiation in these cells.

scholarly journals Osteoporosis in thalassaemia

2018 ◽  
Vol 8 (1) ◽  
Author(s):  
Ersi Voskaridou ◽  
Maria Dimopoulou ◽  
Evangelos Terpos
Keyword(s):  
Bone Resorption ◽  
Nuclear Factor Kappa B ◽  
Human Monoclonal Antibody ◽  
Osteoclast Differentiation ◽  
Osteoclast Formation ◽  
Nuclear Factor ◽  
Receptor Activator ◽  
Formation Function ◽  
And Function ◽  
Markers Of Bone Resorption

Osteoporosis is a prominent cause of morbidity in patients with thalassaemia major (TM) with a complex pathophysiology. Patients with TM and osteoporosis have elevated markers of bone resorption. This increased osteoclast activity seems to be at least partially due to an imbalance in the receptor–activator of nuclear factor-kappa B ligand (RANKL)/osteoprotegerin (OPG) system, which is of great importance for the regulation of osteoclast differentiation and function. Denosumab is a fully human monoclonal antibody that binds to RANKL and thereby inhibits the activation of osteoclasts by RANKL. By blocking RANKL, denosumab inhibits osteoclast formation, function and survival, thereby decreasing bone resorption and increasing bone mass in postmenopausal women and patients with thalassaemia-induced osteoporosis.

scholarly journals Yukmijihwang-Tang Suppresses Receptor Activator of Nuclear Factor Kappa-B Ligand (RANKL)-Induced Osteoclast Differentiation and Prevents Ovariectomy (OVX)-Mediated Bone Loss

Molecules ◽  
2021 ◽  
Vol 26 (24) ◽  
pp. 7579
Author(s):  
Sang-Yong Han ◽  
Yun-Kyung Kim
Keyword(s):  
Bone Loss ◽  
Nuclear Factor Kappa B ◽  
Nuclear Translocation ◽  
Transmembrane Protein ◽  
Osteoclast Differentiation ◽  
Bone Diseases ◽  
Tartrate Resistant Acid Phosphatase ◽  
Nuclear Factor ◽  
Nuclear Factor Kappa ◽  
Receptor Activator

Yukmijihwang-tang (YJ) has been used to treat diabetes mellitus, renal disorders, and cognitive impairment in traditional medicine. This study aimed to evaluate the anti-osteoporotic effect of YJ on ovariectomy (OVX)-induced bone loss in a rat and receptor activator of nuclear factor kappa-B ligand (RANKL)-mediated osteoclast differentiation in bone marrow macrophages (BMMs). YJ reduced the formation of tartrate-resistant acid phosphatase (TRAP)-positive multinucleated cells (MNCs) in an osteoclast/osteoblast co-culture system by regulating the ratio of RANKL/osteoprotegerin (OPG) by osteoblasts. Overall, YJ reduced TRAP-positive cell formation and TRAP activity and F-actin ring formation. Analysis of the underlying mechanisms indicated that YJ inhibited the activation of the nuclear factor of activated T cell cytoplasmic 1 (NFATc1) and c-Fos, resulting in the suppression of osteoclast differentiation-related genes such as TRAP, ATPase, H+ transporting, lysosomal 38 kDa, V0 subunit d2, osteoclast-associated receptor, osteoclast-stimulatory transmembrane protein, dendritic cell-specific transmembrane protein, matrix metalloproteinase-9, cathepsin K, and calcitonin receptor. YJ also inhibited the nuclear translocation of NFATc1. Additionally, YJ markedly inhibited RANKL-induced phosphorylation of signaling pathways activated in the early stages of osteoclast differentiation including the p38, JNK, ERK, and NF-κB. Consistent with these in vitro results, the YJ-administered group showed considerably attenuated bone loss in the OVX-mediated rat model. These results provide promising evidence for the potential novel therapeutic application of YJ for bone diseases such as osteoporosis.

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