OP0088 Discovery of a novel anti-bone resorption compound, AS2690168, which inhibits osteoclastogenesis induced by receptor activator of nuclear factor-kappa B ligand (RANKL)

2013 ◽  
Vol 71 (Suppl 3) ◽  
pp. 125.3-126
Author(s):  
Y. Kato ◽  
N. Morikawa ◽  
E. Hamachi ◽  
H. Nakayama ◽  
Y. Takata ◽  
...  
Keyword(s):  
Bone Resorption ◽  
Nuclear Factor Kappa B ◽  
Nuclear Factor ◽  
Nuclear Factor Kappa ◽  
Receptor Activator

scholarly journals The Molecular Mechanism of Vitamin E as a Bone-Protecting Agent: A Review on Current Evidence

2019 ◽  
Vol 20 (6) ◽  
pp. 1453 ◽  
Author(s):  
Sok Wong ◽  
Nur-Vaizura Mohamad ◽  
Nurul Ibrahim ◽  
Kok-Yong Chin ◽  
Ahmad Shuid ◽  
...  
Keyword(s):  
Vitamin E ◽  
Bone Resorption ◽  
Bone Formation ◽  
Molecular Mechanisms ◽  
Nuclear Factor Kappa B ◽  
Bone Remodelling ◽  
Current Evidence ◽  
Nuclear Factor ◽  
Nuclear Factor Kappa ◽  
Receptor Activator

Bone remodelling is a tightly-coordinated and lifelong process of replacing old damaged bone with newly-synthesized healthy bone. In the bone remodelling cycle, bone resorption is coupled with bone formation to maintain the bone volume and microarchitecture. This process is a result of communication between bone cells (osteoclasts, osteoblasts, and osteocytes) with paracrine and endocrine regulators, such as cytokines, reactive oxygen species, growth factors, and hormones. The essential signalling pathways responsible for osteoclastic bone resorption and osteoblastic bone formation include the receptor activator of nuclear factor kappa-B (RANK)/receptor activator of nuclear factor kappa-B ligand (RANKL)/osteoprotegerin (OPG), Wnt/β-catenin, and oxidative stress signalling. The imbalance between bone formation and degradation, in favour of resorption, leads to the occurrence of osteoporosis. Intriguingly, vitamin E has been extensively reported for its anti-osteoporotic properties using various male and female animal models. Thus, understanding the underlying cellular and molecular mechanisms contributing to the skeletal action of vitamin E is vital to promote its use as a potential bone-protecting agent. This review aims to summarize the current evidence elucidating the molecular actions of vitamin E in regulating the bone remodelling cycle.

Osteoprotegerin (OPG) levels, total soluble receptor activator of nuclear factor-Kappa B ligand (total sRANKL) , and RANKL/OPG ratio in patients with rheumatoid arteritis

2017 ◽  
Vol 2 (1) ◽  
pp. 23-29
Author(s):  
Sousan Kolahi ◽  
Amir Ghorbanihaghjo ◽  
Nadereh Rashtchizadeh ◽  
Alireza Khabbazi ◽  
Mehrzad Hajialilo ◽  
...  
Keyword(s):  
Nuclear Factor Kappa B ◽  
Nuclear Factor ◽  
Soluble Receptor ◽  
Nuclear Factor Kappa ◽  
Receptor Activator

scholarly journals Zinc Sulfate Stimulates Osteogenic Phenotypes in Periosteum-Derived Cells and Co-Cultures of Periosteum-Derived Cells and THP-1 Cells

Life ◽  
2021 ◽  
Vol 11 (5) ◽  
pp. 410
Author(s):  
Jin-Ho Park ◽  
Su A Park ◽  
Young-Hoon Kang ◽  
So Myeong Hwa ◽  
Eun-Byeol Koh ◽  
...  
Keyword(s):  
Bone Resorption ◽  
Zinc Sulfate ◽  
Nuclear Factor Kappa B ◽  
Osteoblastic Differentiation ◽  
Nuclear Factor ◽  
Mitogen Activated Protein Kinases ◽  
Extracellular Signaling ◽  
Receptor Activator ◽  
Mitogen Activated Protein ◽  
Osteoclastic Differentiation

Coupling between osteoblast-mediated bone formation and osteoclast-mediated bone resorption maintains both mechanical integrity and mineral homeostasis. Zinc is required for the formation, mineralization, growth, and maintenance of bones. We examined the effects of zinc sulfate on osteoblastic differentiation of human periosteum-derived cells (hPDCs) and osteoclastic differentiation of THP-1 cells. Zinc sulfate enhanced the osteoblastic differentiation of hPDCs; however, it did not affect the osteoclastic differentiation of THP-1 cells. The levels of extracellular signaling-related kinase (ERK) were strongly increased during osteoblastic differentiation in zinc sulfate-treated hPDCs, compared with other mitogen-activated protein kinases (MAPKs). Zinc sulfate also promoted osteogenesis in hPDCs and THP-1 cells co-cultured with the ratio of one osteoclast to one osteoblast, as indicated by alkaline phosphatase levels, mineralization, and cellular calcium contents. In addition, the receptor activator of nuclear factor kappa B ligand (RANKL)/osteoprotegerin (OPG) ratio was decreased in the zinc sulfate-treated co-cultures. Our results suggest that zinc sulfate enhances osteogenesis directly by promoting osteoblastic differentiation and osteogenic activities in osteoblasts and indirectly by inhibiting osteoclastic bone resorption through a reduced RANKL/OPG ratio in co-cultured osteoblasts and osteoclasts.

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