SF-deferoxamine, a bone-seeking angiogenic drug, prevents bone loss in estrogen-deficient mice

Bone ◽  
2019 ◽  
Vol 120 ◽  
pp. 156-165 ◽  
Author(s):  
Changjun Guo ◽  
Kai Yang ◽  
Yufei Yan ◽  
Dongming Yan ◽  
Yifan Cheng ◽  
...  
Keyword(s):  
Bone Loss ◽  
Deficient Mice

Comparison of the effects of genistein and zoledronic acid on the bone loss in OPG-deficient mice

Bone ◽  
2008 ◽  
Vol 42 (5) ◽  
pp. 950-959 ◽  
Author(s):  
Jianghua Liu ◽  
Kang Xu ◽  
Gebo Wen ◽  
Hui Guo ◽  
San Li ◽  
...  
Keyword(s):  
Zoledronic Acid ◽  
Bone Loss ◽  
Deficient Mice

scholarly journals Accelerated Features of Age-Related Bone Loss in Zmpste24 Metalloproteinase-Deficient Mice

2009 ◽  
Vol 64A (10) ◽  
pp. 1015-1024 ◽  
Author(s):  
D. Rivas ◽  
W. Li ◽  
R. Akter ◽  
J. E. Henderson ◽  
G. Duque
Keyword(s):  
Bone Loss ◽  
Age Related ◽  
Deficient Mice

scholarly journals Klotho-deficient mice are resistant to bone loss induced by unloading due to sciatic neurectomy

2001 ◽  
Vol 168 (2) ◽  
pp. 347-351 ◽  
Author(s):  
T Yamashita ◽  
I Sekiya ◽  
N Kawaguchi ◽  
K Kashimada ◽  
A Nifuji ◽  
...  
Keyword(s):  
Bone Loss ◽  
Cortical Bone ◽  
Gene Product ◽  
Mutant Mice ◽  
Wild Type ◽  
Micro Computed Tomography ◽  
Klotho Gene ◽  
Sciatic Neurectomy ◽  
And Control ◽  
Deficient Mice

Unloading induces bone loss as seen in experimental animals as well as in space flight or in bed-ridden conditions; however, the mechanisms involved in this phenomenon are not fully understood. Klotho mutant mice exhibit osteopetrosis in the metaphyseal regions indicating that the klotho gene product is involved in the regulation of bone metabolism. To examine whether the klotho gene product is involved in the unloading-induced bone loss, the response of the osteopetrotic cancellous bones in these mice was investigated. Sciatic nerve resection was conducted using klotho mutant (kl/kl) and control heterozygous mice (+/kl) and its effect on bone was examined by micro-computed tomography (microCT). As reported previously for wild-type mice (+/+), about 30% bone loss was induced in heterozygous mice (+/kl) by unloading due to neurectomy within 30 days of the surgery. By contrast, kl/kl mice were resistant against bone loss induced by unloading after neurectomy. Unloading due to neurectomy also induced a small but significant bone loss in the cortical bone of the mid-shaft of the femur in the heterozygous mice; no reduction in the cortical bone was observed in kl/kl mice. These results indicate that klotho mutant mice are resistant against bone loss induced by unloading due to neurectomy in both cortical and trabecular bone and indicate that klotho is one of the molecules involved in the loss of bone by unloading.

Involvement of Cot/Tp12 in Bone Loss during Periodontitis

2010 ◽  
Vol 89 (2) ◽  
pp. 192-197 ◽  
Author(s):  
T. Ohnishi ◽  
A. Okamoto ◽  
K. Kakimoto ◽  
K. Bandow ◽  
N. Chiba ◽  
...  
Keyword(s):  
Bone Loss ◽  
Alveolar Bone ◽  
Alveolar Bone Loss ◽  
Periodontal Tissue ◽  
Rankl Expression ◽  
Periodontal Tissues ◽  
Tnf Α ◽  
Experimental Periodontitis ◽  
Deficient Mice

Periodontitis causes resorption of alveolar bone, in which RANKL induces osteoclastogenesis. The binding of lipopolysaccharide to Toll-like receptors causes phosphorylation of Cot/Tp12 to activate the MAPK cascade. Previous in vitro studies showed that Cot/Tp12 was essential for the induction of RANKL expression by lipopolysaccharide. In this study, we examined whether Cot/Tp12 deficiency reduced the progression of alveolar bone loss and osteoclastogenesis during experimental periodontitis. We found that the extent of alveolar bone loss and osteoclastogenesis induced by ligature-induced periodontitis was decreased in Cot/Tp12-deficient mice. In addition, reduction of RANKL expression was observed in periodontal tissues of Cot/Tp12-deficient mice with experimental periodontitis. Furthermore, we found that Cot/Tp12 was involved in the induction of TNF-α mRNA expression in gingiva of mice with experimental periodontitis. Our observations suggested that Cot/Tp12 is essential for the progression of alveolar bone loss and osteoclastogenesis in periodontal tissue during experimental periodontitis mediated through increased RANKL expression.

scholarly journals Treatment of OPG-deficient mice with WP9QY, a RANKL-binding peptide, recovers alveolar bone loss by suppressing osteoclastogenesis and enhancing osteoblastogenesis

PLoS ONE ◽  
2017 ◽  
Vol 12 (9) ◽  
pp. e0184904 ◽  
Author(s):  
Yuki Ozaki ◽  
Masanori Koide ◽  
Yuriko Furuya ◽  
Tadashi Ninomiya ◽  
Hisataka Yasuda ◽  
...  
Keyword(s):  
Bone Loss ◽  
Alveolar Bone ◽  
Alveolar Bone Loss ◽  
Binding Peptide ◽  
Deficient Mice

A protective effect of Curcuma comosa Roxb. on bone loss in estrogen deficient mice

2011 ◽  
Vol 137 (2) ◽  
pp. 956-962 ◽  
Author(s):  
Jittima Weerachayaphorn ◽  
Aporn Chuncharunee ◽  
Chitrawina Mahagita ◽  
Buarong Lewchalermwongse ◽  
Apichart Suksamrarn ◽  
...  
Keyword(s):  
Bone Loss ◽  
Protective Effect ◽  
Curcuma Comosa ◽  
Deficient Mice

IL-6 is not required for parathyroid hormone stimulation of RANKL expression, osteoclast formation, and bone loss in mice

2005 ◽  
Vol 289 (5) ◽  
pp. E784-E793 ◽  
Author(s):  
Charles A. O'Brien ◽  
Robert L. Jilka ◽  
Qiang Fu ◽  
Scott Stewart ◽  
Robert S. Weinstein ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Bone Loss ◽  
Secondary Hyperparathyroidism ◽  
Osteoclast Formation ◽  
Luciferase Reporter ◽  
Wild Type ◽  
Deficient Diet ◽  
Rankl Mrna ◽  
Deficient Mice

Continuous elevation of parathyroid hormone (PTH) increases osteoclast precursors, the number of osteoclasts on cancellous bone, and bone turnover. The essential molecular mediators of these effects are controversial, however, and both increased receptor activator of NF-κB ligand (RANKL) and IL-6 have been implicated. The goal of these studies was to determine whether continuous elevation of endogenous PTH alters IL-6 gene expression in vivo and whether IL-6 is required for PTH-induced bone loss. To accomplish this, we generated transgenic mice harboring a luciferase reporter gene under the control of IL-6 gene regulatory regions to allow accurate quantification of IL-6 gene activity in vivo. In these mice, induction of secondary hyperparathyroidism using a calcium-deficient diet did not alter IL-6-luciferase transgene expression, whereas RANKL mRNA expression was elevated in bone tissue. Moreover, secondary hyperparathyroidism induced an equivalent amount of bone loss in wild-type and IL-6-deficient mice, and PTH elevated RANKL mRNA and osteoclast formation to the same extent in bone marrow cultures derived from wild-type and IL-6-deficient mice. These results demonstrate that IL-6 is not required for the osteoclast formation and bone loss that accompanies continuous elevation of PTH.

scholarly journals Interleukin-6 deficient mice are protected from bone loss caused by estrogen depletion.

1994 ◽  
Vol 13 (5) ◽  
pp. 1189-1196 ◽  
Author(s):  
V. Poli ◽  
R. Balena ◽  
E. Fattori ◽  
A. Markatos ◽  
M. Yamamoto ◽  
...  
Keyword(s):  
Bone Loss ◽  
Interleukin 6 ◽  
Estrogen Depletion ◽  
Deficient Mice

scholarly journals Resistance to Unloading-Induced Three-Dimensional Bone Loss in Osteopontin-Deficient Mice

2002 ◽  
Vol 17 (4) ◽  
pp. 661-667 ◽  
Author(s):  
Muneaki Ishijima ◽  
Kunikazu Tsuji ◽  
Susan R. Rittling ◽  
Teruhito Yamashita ◽  
Hisashi Kurosawa ◽  
...  
Keyword(s):  
Bone Loss ◽  
Three Dimensional ◽  
Deficient Mice
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