scholarly journals Conditional deletion of Bmpr1a in differentiated osteoclasts increases osteoblastic bone formation, increasing volume of remodeling bone in mice

2011 ◽  
Vol 26 (10) ◽  
pp. 2511-2522 ◽  
Author(s):  
Mina Okamoto ◽  
Junko Murai ◽  
Yuuki Imai ◽  
Daisuke Ikegami ◽  
Nobuhiro Kamiya ◽  
...  
Keyword(s):  
Bone Formation ◽  
Conditional Deletion ◽  
Osteoblastic Bone Formation

scholarly journals MiR‐103‐3p targets the m 6 A methyltransferase METTL14 to inhibit osteoblastic bone formation

Aging Cell ◽  
2021 ◽  
Vol 20 (2) ◽  
Author(s):  
Zhongyang Sun ◽  
Han Wang ◽  
Yuxiang Wang ◽  
Guodong Yuan ◽  
Xin Yu ◽  
...  
Keyword(s):  
Bone Formation ◽  
Osteoblastic Bone Formation

Fine-tuning between BMP and NF-κB pathways regulates osteoblastic bone formation

2016 ◽  
Vol 58 (3) ◽  
pp. 73-77 ◽  
Author(s):  
Shizu Hirata-Tsuchiya ◽  
Hidefumi Fukushima ◽  
Shoichiro Kokabu ◽  
Chiaki Kitamura ◽  
Eijiro Jimi
Keyword(s):  
Bone Formation ◽  
Fine Tuning ◽  
Osteoblastic Bone Formation

scholarly journals Novel Osteogenic Factors derived from Functional Food: Role in Prevention of Osteoporosis

2015 ◽  
Vol 1 (1) ◽  
Author(s):  
Masayoshi Yamaguchi
Keyword(s):  
Bone Resorption ◽  
Bone Loss ◽  
Bone Formation ◽  
Functional Food ◽  
Human Subjects ◽  
Osteoclastic Bone Resorption ◽  
Bone Homeostasis ◽  
Osteoblastic Bone Formation ◽  
Prevention Of Osteoporosis ◽  
Osteogenic Effect

<p>Bone homeostasis is maintained through a delicate balance between osteoblastic bone formation and osteoclastic bone resorption. Bone loss is caused by decreasing in osteoblastic bone formation and increase in osteoclastic bone resorption, thereby leading to osteoporosis. Functional food factors may play a role in<br />the prevention of osteoporosis. Functional food factors including genistein, menaquinone-7 (vitamin K2) and β-cryptoxanthine have been shown to possess a potential osteogenic effect. These factors have been shown to reveal stimulatory effects on osteoblastic bone formation and suppressive effects on osteoclastic<br />bone resorption. Dietary intake of these factors has been shown to reveal preventive effects on bone loss in animal models of osteoporosis and human subjects. This review will introduce our findings concerning roles of functional food factors in regulation of bone homeostasis and prevention of osteoporosis.</p>

scholarly journals Cthrc1 Is a Positive Regulator of Osteoblastic Bone Formation

PLoS ONE ◽  
2008 ◽  
Vol 3 (9) ◽  
pp. e3174 ◽  
Author(s):  
Hiroaki Kimura ◽  
Kin Ming Kwan ◽  
Zhaoping Zhang ◽  
Jian Min Deng ◽  
Bryant G. Darnay ◽  
...  
Keyword(s):  
Bone Formation ◽  
Positive Regulator ◽  
Osteoblastic Bone Formation

scholarly journals Enhancement of Osteoclastic Bone Resorption and Suppression of Osteoblastic Bone Formation in Response to Reduced Mechanical Stress Do Not Occur in the Absence of Osteopontin

2001 ◽  
Vol 193 (3) ◽  
pp. 399-404 ◽  
Author(s):  
Muneaki Ishijima ◽  
Susan R. Rittling ◽  
Teruhito Yamashita ◽  
Kunikazu Tsuji ◽  
Hisashi Kurosawa ◽  
...  
Keyword(s):  
Bone Resorption ◽  
Bone Loss ◽  
Bone Formation ◽  
Mechanical Stress ◽  
Bone Matrix ◽  
Osteoclastic Bone Resorption ◽  
Tail Suspension ◽  
Wild Type ◽  
Osteoblastic Bone Formation

Reduced mechanical stress to bone in bedridden patients and astronauts leads to bone loss and increase in fracture risk which is one of the major medical and health issues in modern aging society and space medicine. However, no molecule involved in the mechanisms underlying this phenomenon has been identified to date. Osteopontin (OPN) is one of the major noncollagenous proteins in bone matrix, but its function in mediating physical-force effects on bone in vivo has not been known. To investigate the possible requirement for OPN in the transduction of mechanical signaling in bone metabolism in vivo, we examined the effect of unloading on the bones of OPN−/− mice using a tail suspension model. In contrast to the tail suspension–induced bone loss in wild-type mice, OPN−/− mice did not lose bone. Elevation of urinary deoxypyridinoline levels due to unloading was observed in wild-type but not in OPN−/− mice. Analysis of the mechanisms of OPN deficiency–dependent reduction in bone on the cellular basis resulted in two unexpected findings. First, osteoclasts, which were increased by unloading in wild-type mice, were not increased by tail suspension in OPN−/− mice. Second, measures of osteoblastic bone formation, which were decreased in wild-type mice by unloading, were not altered in OPN−/− mice. These observations indicate that the presence of OPN is a prerequisite for the activation of osteoclastic bone resorption and for the reduction in osteoblastic bone formation in unloaded mice. Thus, OPN is a molecule required for the bone loss induced by mechanical stress that regulates the functions of osteoblasts and osteoclasts.

Conditional deletion of Indian hedgehog from collagen type 2α1-expressing cells results in abnormal endochondral bone formation

2005 ◽  
Vol 207 (4) ◽  
pp. 453-461 ◽  
Author(s):  
Mohammed S Razzaque ◽  
Desi W Soegiarto ◽  
Da Chang ◽  
Fanxin Long ◽  
Beate Lanske
Keyword(s):  
Bone Formation ◽  
Collagen Type ◽  
Indian Hedgehog ◽  
Endochondral Bone Formation ◽  
Endochondral Bone ◽  
Conditional Deletion

scholarly journals The orphan nuclear receptor SHP is a positive regulator of osteoblastic bone formation

2009 ◽  
Vol 25 (2) ◽  
pp. 262-274 ◽  
Author(s):  
Byung-Chul Jeong ◽  
Yong-Soo Lee ◽  
In-Ho Bae ◽  
Chul-Ho Lee ◽  
Hong-In Shin ◽  
...  
Keyword(s):  
Bone Formation ◽  
Nuclear Receptor ◽  
Orphan Nuclear Receptor ◽  
Positive Regulator ◽  
Osteoblastic Bone Formation

scholarly journals CHMP5 controls bone turnover rates by dampening NF-κB activity in osteoclasts

2015 ◽  
Vol 212 (8) ◽  
pp. 1283-1301 ◽  
Author(s):  
Matthew B. Greenblatt ◽  
Kwang Hwan Park ◽  
Hwanhee Oh ◽  
Jung-Min Kim ◽  
Dong Yeon Shin ◽  
...  
Keyword(s):  
Bone Resorption ◽  
Bone Formation ◽  
Bone Turnover ◽  
Osteoclast Differentiation ◽  
Multivesicular Body ◽  
Deubiquitinating Enzyme ◽  
Turnover Rates ◽  
Body Protein ◽  
Conditional Deletion ◽  
Tightly Coupled

Physiological bone remodeling requires that bone formation by osteoblasts be tightly coupled to bone resorption by osteoclasts. However, relatively little is understood about how this coupling is regulated. Here, we demonstrate that modulation of NF-κB signaling in osteoclasts via a novel activity of charged multivesicular body protein 5 (CHMP5) is a key determinant of systemic rates of bone turnover. A conditional deletion of CHMP5 in osteoclasts leads to increased bone resorption by osteoclasts coupled with exuberant bone formation by osteoblasts, resembling an early onset, polyostotic form of human Paget’s disease of bone (PDB). These phenotypes are reversed by haploinsufficiency for Rank, as well as by antiresorptive treatments, including alendronate, zolendronate, and OPG-Fc. Accordingly, CHMP5-deficient osteoclasts display increased RANKL-induced NF-κB activation and osteoclast differentiation. Biochemical analysis demonstrated that CHMP5 cooperates with the PDB genetic risk factor valosin-containing protein (VCP/p97) to stabilize the inhibitor of NF-κBα (IκBα), down-regulating ubiquitination of IκBα via the deubiquitinating enzyme USP15. Thus, CHMP5 tunes NF-κB signaling downstream of RANK in osteoclasts to dampen osteoclast differentiation, osteoblast coupling and bone turnover rates, and disruption of CHMP5 activity results in a PDB-like skeletal disorder.

scholarly journals Synergistic effects of high dietary calcium and exogenous parathyroid hormone in promoting osteoblastic bone formation in mice

2015 ◽  
Vol 113 (6) ◽  
pp. 909-922 ◽  
Author(s):  
Yuxu Feng ◽  
Min Zhou ◽  
Qunhu Zhang ◽  
Huan Liu ◽  
Yong Xu ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Treatment Group ◽  
Bone Formation ◽  
Synergistic Effects ◽  
Type I ◽  
Osteoblast Proliferation ◽  
Mineral Density ◽  
Expression Levels ◽  
Osteoblastic Bone Formation ◽  
Proliferation And Differentiation

In the present study, we investigated whether high dietary Ca and exogenous parathyroid hormone 1–34 fragments (PTH 1–34) have synergistic effects on bone formation in adult mice, and explored the related mechanisms. Adult male mice were fed a normal diet, a high-Ca diet, a PTH-treated diet, or a high-Ca diet combined with subcutaneously injected PTH 1–34 (80 μg/kg per d) for 4 weeks. Bone mineral density, trabecular bone volume, osteoblast number, alkaline phosphatase (ALP)- and type I collagen-positive areas, and the expression levels of osteoblastic bone formation-related genes and proteins were increased significantly in mice fed the high-Ca diet, the PTH-treated diet, and, even more dramatically, the high-Ca diet combined with PTH. Osteoclast number and surface and the ratio of receptor activator for nuclear factor-κB ligand (RANKL):osteoprotegerin (OPG) were decreased in the high-Ca diet treatment group, increased in the PTH treatment group, but not in the combined treatment group. Furthermore, third-passage osteoblasts were treated with high Ca (5 mm), PTH 1–34 (10− 8m) or high Ca combined with PTH 1–34. Osteoblast viability and ALP activity were increased in either the high Ca-treated or PTH-treated cultures and, even more dramatically, in the cultures treated with high Ca plus PTH, with consistent up-regulation of the expression levels of osteoblast proliferation and differentiation-related genes and proteins. These results indicate that dietary Ca and PTH play synergistic roles in promoting osteoblastic bone formation by stimulating osteoblast proliferation and differentiation.

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