Intrauterine stress induces bone loss in adult offspring of C3H/HeJ mice having high bone mass phenotype but not C57BL/6J mice with low bone mass phenotype

Bone ◽  
2016 ◽  
Vol 87 ◽  
pp. 114-119 ◽  
Author(s):  
M. Raygorodskaya ◽  
Y. Gabet ◽  
C. Shochat ◽  
E. Kobyliansky ◽  
A. Torchinsky ◽  
...  
Keyword(s):  
Bone Loss ◽  
Bone Mass ◽  
Adult Offspring ◽  
Low Bone Mass ◽  
High Bone Mass ◽  
High Bone ◽  
High Bone Mass Phenotype

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 Mice lacking DKK1 in T cells exhibit high bone mass and are protected from estrogen deficiency-induced bone loss

iScience ◽  
2021 ◽  
pp. 102224
Author(s):  
Juliane Lehmann ◽  
Sylvia Thiele ◽  
Ulrike Baschant ◽  
Tilman D. Rachner ◽  
Christof Niehrs ◽  
...  
Keyword(s):  
T Cells ◽  
Bone Loss ◽  
Bone Mass ◽  
Estrogen Deficiency ◽  
High Bone Mass ◽  
High Bone

scholarly journals Sex dimorphic regulation of osteoprogenitor progesterone in bone stromal cells

2017 ◽  
Vol 59 (4) ◽  
pp. 351-363 ◽  
Author(s):  
Alexander Kot ◽  
Zhendong A Zhong ◽  
Hongliang Zhang ◽  
Yu-An Evan Lay ◽  
Nancy E Lane ◽  
...  
Keyword(s):  
Mouse Model ◽  
Bone Mass ◽  
Gene Transcription ◽  
Conditional Knockout ◽  
Sequencing Analysis ◽  
Wild Type ◽  
High Bone Mass ◽  
Matrix Interaction ◽  
High Bone ◽  
High Bone Mass Phenotype

Increasing peak bone mass is a promising strategy to prevent osteoporosis. A mouse model of global progesterone receptor (PR) ablation showed increased bone mass through a sex-dependent mechanism. Cre-Lox recombination was used to generate a mouse model of osteoprogenitor-specific PR inactivation, which recapitulated the high bone mass phenotype seen in the PR global knockout mouse mode. In this work, we employed RNA sequencing analysis to evaluate sex-independent and sex-dependent differences in gene transcription of osteoprogenitors of wild-type and PR conditional knockout mice. PR deletion caused marked sex hormone-dependent changes in gene transcription in male mice as compared to wild-type controls. These transcriptional differences revealed dysregulation in pathways involving immunomodulation, osteoclasts, bone anabolism, extracellular matrix interaction and matrix interaction. These results identified many potential mechanisms that may explain our observed high bone mass phenotype with sex differences when PR was selectively deleted in the MSCs.

scholarly journals Novel LRP5 Missense Mutation in a Patient With a High Bone Mass Phenotype Results in Decreased DKK1-Mediated Inhibition of Wnt Signaling*

2007 ◽  
Vol 22 (5) ◽  
pp. 708-716 ◽  
Author(s):  
Wendy Balemans ◽  
Jean-Pierre Devogelaer ◽  
Erna Cleiren ◽  
Elke Piters ◽  
Emanuelle Caussin ◽  
...  
Keyword(s):  
Bone Mass ◽  
Wnt Signaling ◽  
Missense Mutation ◽  
High Bone Mass ◽  
High Bone ◽  
High Bone Mass Phenotype

NFATC2-knock-out mice reveal a high bone mass phenotype

Bone ◽  
2010 ◽  
Vol 47 ◽  
pp. S40
Author(s):  
M. Rauner⁎ ◽  
W. Bauer ◽  
I. Habermann ◽  
M. Haase ◽  
C. Goettsch ◽  
...  
Keyword(s):  
Bone Mass ◽  
High Bone Mass ◽  
Knock Out ◽  
High Bone ◽  
High Bone Mass Phenotype ◽  
Knock Out Mice

scholarly journals Commentary-FSH and bone 2010: evolving evidence

2010 ◽  
Vol 163 (1) ◽  
pp. 173-176 ◽  
Author(s):  
Jameel Iqbal ◽  
Li Sun ◽  
Mone Zaidi
Keyword(s):  
Bone Loss ◽  
Bone Mass ◽  
Current Issue ◽  
Scientific Evidence ◽  
Primary Role ◽  
Low Bone Mass ◽  
Genetic Studies ◽  
High Bone ◽  
Estrogen Effect

Bone loss due to menopause, natural or artificial, has been attributed solely to low estrogen. However, in a woman's life, the most precipitous bone loss begins 2 years prior to the last menstrual period, during which time estrogen levels are unperturbed whereas FSH is elevated. Our cell-based and mouse genetic studies have shown that FSH stimulates bone resorption by osteoclasts directly in a pituitary–bone axis, independently of the estrogen effect. On the basis of this and evolving clinical and scientific evidence, we propose that elevated FSH contributes to bone loss across the menopausal transition, particularly during late perimenopause. In the current issue of theEuropean Journal of Endocrinology, Rendinaet al.strengthen the view for a primary role of FSH signaling in the regulation of bone mass and bone remodeling in humans by demonstrating that an ‘activating’ polymorphism AA rs6166 causes low bone mass and high bone turnover.

scholarly journals Cocaine and Amphetamine-Regulated Transcript May Regulate Bone Remodeling as a Circulating Molecule

Endocrinology ◽  
2008 ◽  
Vol 149 (8) ◽  
pp. 3933-3941 ◽  
Author(s):  
Manvendra K. Singh ◽  
Florent Elefteriou ◽  
Gerard Karsenty
Keyword(s):  
Bone Mass ◽  
Bone Remodeling ◽  
Third Ventricle ◽  
Fold Increase ◽  
Low Bone Mass ◽  
High Bone Mass ◽  
Peripheral Tissues ◽  
Osteoclast Number ◽  
High Bone ◽  
The Brain

Cocaine- and amphetamine-regulated transcript (CART) is one of the two known mediators of the leptin regulation of bone mass. Cart is expressed in both the brain and peripheral tissues such as the pituitary gland and the pancreatic islets. Cart−/− mice present a low bone mass phenotype due to an isolated increase in osteoclast number. In an effort to rescue their bone phenotype, we delivered recombinant CART in the third ventricle of the mutant mice but never recorded any improvement of the low bone mass, although this procedure could affect fat pad mass. In contrast, transgenic mice harboring a 2-fold increase in CART circulating level display a high bone mass due to an isolated decrease in osteoclast number and could rescue the low bone mass phenotype of the Cart−/− mice. Thus, our results suggest that in its capacity of a regulator of bone remodeling, CART may act more as a circulating molecule than a neuropeptide.

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