scholarly journals NELL-1 in the treatment of osteoporotic bone loss

2015 ◽  
Vol 6 (1) ◽  
Author(s):  
Aaron W. James ◽  
Jia Shen ◽  
Xinli Zhang ◽  
Greg Asatrian ◽  
Raghav Goyal ◽  
...  
Keyword(s):  
Biomaterials ◽  
2021 ◽  
pp. 120819
Author(s):  
Jiaul Hoque ◽  
Yu-Ru V. Shih ◽  
Yuze Zeng ◽  
Hunter Newman ◽  
Nivedita Sangaj ◽  
...  

PLoS ONE ◽  
2018 ◽  
Vol 13 (9) ◽  
pp. e0202885 ◽  
Author(s):  
JiaXin Bei ◽  
XinLe Zhang ◽  
JingKai Wu ◽  
ZhuoQing Hu ◽  
BiLian Xu ◽  
...  

JBMR Plus ◽  
2019 ◽  
Vol 3 (12) ◽  
Author(s):  
Zeeshan Sheikh ◽  
Gang Chen ◽  
Faik Al‐Jaf ◽  
Marion Thévenin ◽  
Kate Banks ◽  
...  

2019 ◽  
Vol 5 (8) ◽  
pp. eaax1387 ◽  
Author(s):  
Yu-Ru V. Shih ◽  
Mengqian Liu ◽  
Seong Keun Kwon ◽  
Masayuki Iida ◽  
Ya Gong ◽  
...  

Adenosine and its receptors play a key role in bone homeostasis and regeneration. Extracellular adenosine is generated from CD39 and CD73 activity in the cell membrane, through conversion of adenosine triphosphate to adenosine monophosphate (AMP) and AMP to adenosine, respectively. Despite the relevance of CD39/CD73 to bone health, the roles of these enzymes in bona fide skeletal disorders remain unknown. We demonstrate that CD39/CD73 expression and extracellular adenosine levels in the bone marrow are substantially decreased in animals with osteoporotic bone loss. Knockdown of estrogen receptors ESR1 and ESR2 in primary osteoprogenitors and osteoclasts undergoing differentiation showed decreased coexpression of membrane-bound CD39 and CD73 and lower extracellular adenosine. Targeting the adenosine A2B receptor using an agonist attenuated bone loss in ovariectomized mice. Together, these findings suggest a pathological association of purine metabolism with estrogen deficiency and highlight the potential of A2B receptor as a target to treat osteoporosis.


Nutrients ◽  
2020 ◽  
Vol 12 (11) ◽  
pp. 3565
Author(s):  
Eunkuk Park ◽  
Jeonghyun Kim ◽  
Hyun-Seok Jin ◽  
Chun Whan Choi ◽  
Tae Hyun Choi ◽  
...  

Bone remodeling is a renewal process regulated by bone synthesis (osteoblasts) and bone destruction (osteoclasts). A previous study demonstrated that Lycii radicis cortex (LRC) extract inhibited ovariectomized (OVX)-induced bone loss in mice. This study investigated the anti-osteoporotic effects of bioactive constituent(s) from the LRC extract. The effective compound(s) were screened, and a single compound, scopolin, which acts as a phytoalexin, was chosen as a candidate component. Scopolin treatment enhanced alkaline phosphatase activity and increased mineralized nodule formation in MC3T3-E1 pre-osteoblastic cells. However, osteoclast differentiation in primary-cultured monocytes was reduced by treatment with scopolin. Consistently, scopolin treatment increased osteoblast differentiation in the co-culture of monocytes (osteoclasts) and MC3T3-E1 (osteoblast) cells. Scopolin treatment prevented bone mineral density loss in OVX-induced osteoporotic mice. These results suggest that scopolin could be a therapeutic bioactive constituent for the treatment and prevention of osteoporosis.


2011 ◽  
Vol 208 (9) ◽  
pp. 1849-1861 ◽  
Author(s):  
Yu-Hsiang Hsu ◽  
Wei-Yu Chen ◽  
Chien-Hui Chan ◽  
Chih-Hsing Wu ◽  
Zih-Jie Sun ◽  
...  

IL-20 is a proinflammatory cytokine of the IL-10 family that is involved in psoriasis, rheumatoid arthritis, atherosclerosis, and stroke. However, little is known about the role of IL-20 in bone destruction. We explored the function of IL-20 in osteoclastogenesis and the therapeutic potential of anti–IL-20 monoclonal antibody 7E for treating osteoporosis. Higher serum IL-20 levels were detected in patients with osteopenia and osteoporosis and in ovariectomized (OVX) mice. IL-20 mediates osteoclastogenesis by up-regulating the receptor activator of NF-κB (RANK) expression in osteoclast precursor cells and RANK ligand (RANKL) in osteoblasts. 7E treatment completely inhibited osteoclast differentiation induced by macrophage colony-stimulating factor (M-CSF) and RANKL in vitro and protected mice from OVX-induced bone loss in vivo. Furthermore, IL-20R1–deficient mice had significantly higher bone mineral density (BMD) than did wild-type controls. IL-20R1 deficiency also abolished IL-20–induced osteoclastogenesis and increased BMD in OVX mice. We have identified a pivotal role of IL-20 in osteoclast differentiation, and we conclude that anti–IL-20 monoclonal antibody is a potential therapeutic for protecting against osteoporotic bone loss.


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