Deletion of hypothalamic neuropeptide Y2-receptors in adult mice protects against continued ovariectomy-induced bone loss

Bone ◽  
2006 ◽  
Vol 38 (3) ◽  
pp. 6
Author(s):  
S.J. Allison ◽  
P.A. Baldock ◽  
A. Sainsbury ◽  
R.F. Enriquez ◽  
M. During ◽  
...  
Keyword(s):  
Bone Loss ◽  
Adult Mice

Serotonin (5-hydroxytryptamine) transporter inhibition causes bone loss in adult mice independently of estrogen deficiency

2008 ◽  
Vol 15 (6) ◽  
pp. 1176-1183 ◽  
Author(s):  
Stuart J. Warden ◽  
Ian R. Nelson ◽  
Robyn K. Fuchs ◽  
Michael M. Bliziotes ◽  
Charles H. Turner
Keyword(s):  
Bone Loss ◽  
Estrogen Deficiency ◽  
Adult Mice

scholarly journals Soluble RANKL contributes to osteoclast formation in adult mice but not ovariectomy-induced bone loss

2018 ◽  
Vol 9 (1) ◽  
Author(s):  
Jinhu Xiong ◽  
Keisha Cawley ◽  
Marilina Piemontese ◽  
Yuko Fujiwara ◽  
Haibo Zhao ◽  
...  
Keyword(s):  
Bone Loss ◽  
Osteoclast Formation ◽  
Adult Mice

scholarly journals RANKL from Bone Marrow Adipocytes Regulates Osteoclast Formation and Bone Loss in Mice

2020 ◽  
Author(s):  
Xin Zhi ◽  
Yan Hu ◽  
Xiaoqun Li ◽  
Wei Cong ◽  
Biaotong Huang ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Bone Loss ◽  
Cancellous Bone ◽  
Osteoclast Formation ◽  
Adult Mice ◽  
Conditional Deletion ◽  
Bone Marrow Adipocytes ◽  
Calcified Cartilage ◽  
Cellular Source ◽  
Trabecular Bone Loss

AbstractReceptor activator of NF-κB ligand (RANKL) is essential for osteoclast formation. The cellular source of RANKL for osteoclastogenesis has not been fully uncovered. Bone marrow (BM) adipocytes derived from bone marrow mesenchymal stromal cells (BMSCs) express RANKL. Here we demonstrated that the AdipoqCre could target bone marrow adipocytes. We crossed the AdipoqCre mice with ranklfl/fl mice to conditionally delete RANKL from BM adipocytes. Conditional deletion of RANKL increased cancellous bone mass in the long bones of growing and adult mice by reducing the formation of trabecular osteoclasts and inhibiting bone resorption but did not affect cortical bone thickness or resorption of calcified cartilage. AdipoqCre; ranklfl/fl mice exhibited resistance to estrogen deficiency and rosiglitazone (ROS) induced trabecular bone loss but showed bone loss induced by unloading. BM adipocytes therefore represent an essential source of RANKL for the formation of trabecula osteoclasts and resorption of cancellous bone during remodeling.

scholarly journals The RANKL Distal Control Region Is Required for the Increase in RANKL Expression, But Not the Bone Loss, Associated with Hyperparathyroidism or Lactation in Adult Mice

2012 ◽  
Vol 26 (2) ◽  
pp. 341-348 ◽  
Author(s):  
Melda Onal ◽  
Carlo Galli ◽  
Qiang Fu ◽  
Jinhu Xiong ◽  
Robert S. Weinstein ◽  
...  
Keyword(s):  
Bone Resorption ◽  
Bone Loss ◽  
Control Region ◽  
Dominant Role ◽  
Dietary Calcium ◽  
Calcium Deficiency ◽  
Wild Type ◽  
Rankl Expression ◽  
Adult Mice ◽  
Dietary Calcium Deficiency

Abstract Osteoclast-mediated bone resorption plays an essential role in calcium homeostasis and lactation. The cytokine receptor activator of nuclear factor κB ligand (RANKL) is one of a number of factors that controls the production, survival, and activity of osteoclasts. Calciotropic hormones, such as PTH, control RANKL transcription in part via an enhancer known as the distal control region (DCR), and mice lacking this enhancer have fewer osteoclasts under normal physiological conditions. Here, we have addressed the role of the DCR in situations in which activation of the PTH receptor is thought to stimulate bone resorption via elevation of RANKL expression. Dietary calcium deficiency stimulated RANKL expression in the bone of young (1 month old) wild-type, but not DCR knockout (KO), mice. Consistent with this, the cancellous bone loss and the increase in osteoclasts caused by dietary calcium deficiency were blunted in young KO mice. DCR deletion also prevented the increase in RANKL expression caused by dietary calcium deficiency in 6-month-old mice. However, the diet-induced bone loss was similar in wild-type and KO mice at this age. The increase in RANKL expression caused by lactation was also blunted in DCR KO mice, but lactation-induced bone loss was similar in both genotypes. These results demonstrate that, even though the DCR is required for the increase in RANKL expression associated with hyperparathyroidism or lactation, this increase is not required for the bone loss caused by these conditions in adult mice, suggesting that changes in other factors, such as osteoprotegerin or estrogen levels, play a dominant role.

Antenatal glucocorticoid injections do not aggravate stress-induced bone loss in young adult mice

2013 ◽  
Author(s):  
Henneicke Holger ◽  
J Gasparini Sylvia ◽  
C Brennan-Speranza Tara ◽  
Zhou Hong ◽  
J Seibel Markus
Keyword(s):  
Young Adult ◽  
Bone Loss ◽  
Adult Mice

scholarly journals (−)-Epiafzelechin Protects against Ovariectomy-induced Bone Loss in Adult Mice and Modulate Osteoblastic and Osteoclastic Functions In Vitro

Nutrients ◽  
2017 ◽  
Vol 9 (5) ◽  
pp. 530 ◽  
Author(s):  
Ka-Chun Wong ◽  
Sisi Cao ◽  
Xiaoli Dong ◽  
Man-Chun Law ◽  
Tak-Hang Chan ◽  
...  
Keyword(s):  
Bone Loss ◽  
Adult Mice

scholarly journals Inactivation ofVhlin Osteochondral Progenitor Cells Causes High Bone Mass Phenotype and Protects Against Age-Related Bone Loss in Adult Mice

2014 ◽  
Vol 29 (4) ◽  
pp. 820-829 ◽  
Author(s):  
Tujun Weng ◽  
Yangli Xie ◽  
Junlan Huang ◽  
Fengtao Luo ◽  
Lingxian Yi ◽  
...  
Keyword(s):  
Bone Loss ◽  
Bone Mass ◽  
Progenitor Cells ◽  
High Bone Mass ◽  
Adult Mice ◽  
Age Related ◽  
High Bone ◽  
High Bone Mass Phenotype

scholarly journals Induction of somatopause in adult mice compromises bone morphology and exacerbates bone loss during aging

Aging Cell ◽  
2021 ◽  
Author(s):  
Manisha Dixit ◽  
Silvana Duran‐Ortiz ◽  
Godze Yildirim ◽  
Sher Bahadur Poudel ◽  
Leeann D. Louis ◽  
...  
Keyword(s):  
Bone Loss ◽  
Bone Morphology ◽  
Adult Mice
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