scholarly journals Load-induced changes in bone stiffness and cancellous and cortical bone mass following tibial compression diminish with age in female mice

2014 ◽  
Vol 217 (10) ◽  
pp. 1775-1783 ◽  
Author(s):  
R. P. Main ◽  
M. E. Lynch ◽  
M. C. H. van der Meulen
Keyword(s):  
Bone Mass ◽  
Cortical Bone ◽  
Bone Stiffness ◽  
Female Mice ◽  
Cortical Bone Mass ◽  
Induced Changes

scholarly journals Female Mice Lacking Estrogen Receptor-α in Hypothalamic Proopiomelanocortin (POMC) Neurons Display Enhanced Estrogenic Response on Cortical Bone Mass

Endocrinology ◽  
2016 ◽  
Vol 157 (8) ◽  
pp. 3242-3252 ◽  
Author(s):  
H. H. Farman ◽  
S. H. Windahl ◽  
L. Westberg ◽  
H. Isaksson ◽  
E. Egecioglu ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Bone Mass ◽  
Mechanical Strength ◽  
Cortical Bone ◽  
Volume Fraction ◽  
Bone Thickness ◽  
Female Mice ◽  
Cortical Bone Thickness ◽  
Cortical Bone Mass ◽  
Estrogenic Responses

Estrogens are important regulators of bone mass and their effects are mainly mediated via estrogen receptor (ER)α. Central ERα exerts an inhibitory role on bone mass. ERα is highly expressed in the arcuate (ARC) and the ventromedial (VMN) nuclei in the hypothalamus. To test whether ERα in proopiomelanocortin (POMC) neurons, located in ARC, is involved in the regulation of bone mass, we used mice lacking ERα expression specifically in POMC neurons (POMC-ERα−/−). Female POMC-ERα−/− and control mice were ovariectomized (OVX) and treated with vehicle or estradiol (0.5 μg/d) for 6 weeks. As expected, estradiol treatment increased the cortical bone thickness in femur, the cortical bone mechanical strength in tibia and the trabecular bone volume fraction in both femur and vertebrae in OVX control mice. Importantly, the estrogenic responses were substantially increased in OVX POMC-ERα−/− mice compared with the estrogenic responses in OVX control mice for cortical bone thickness (+126 ± 34%, P < .01) and mechanical strength (+193 ± 38%, P < .01). To test whether ERα in VMN is involved in the regulation of bone mass, ERα was silenced using an adeno-associated viral vector. Silencing of ERα in hypothalamic VMN resulted in unchanged bone mass. In conclusion, mice lacking ERα in POMC neurons display enhanced estrogenic response on cortical bone mass and mechanical strength. We propose that the balance between inhibitory effects of central ERα activity in hypothalamic POMC neurons in ARC and stimulatory peripheral ERα-mediated effects in bone determines cortical bone mass in female mice.

scholarly journals Deletion of Estrogen Receptor Beta in Osteoprogenitor Cells Increases Trabecular but Not Cortical Bone Mass in Female Mice

2015 ◽  
Vol 31 (3) ◽  
pp. 606-614 ◽  
Author(s):  
Kristy M Nicks ◽  
Koji Fujita ◽  
Daniel Fraser ◽  
Ulrike McGregor ◽  
Matthew T Drake ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Bone Mass ◽  
Cortical Bone ◽  
Estrogen Receptor Beta ◽  
Osteoprogenitor Cells ◽  
Female Mice ◽  
Cortical Bone Mass ◽  
Receptor Beta

Effects of long-term sedentary behaviour on the cortical bone mass and distribution during growth: The HAPPY bone study

2017 ◽  
Author(s):  
Rachel L Duckham ◽  
Timo Rantalainen ◽  
Christine Rodda ◽  
Anna Timperio ◽  
Nicola Hawley ◽  
...  
Keyword(s):  
Bone Mass ◽  
Cortical Bone ◽  
Sedentary Behaviour ◽  
Cortical Bone Mass

scholarly journals Deletion of Rptor in pre‐osteoblasts reveals a role for the mTORC1 complex in dietary‐induced changes to bone mass and glucose homeostasis in female mice

JBMR Plus ◽  
2021 ◽  
Author(s):  
Pawanrat Tangseefa ◽  
Sally K. Martin ◽  
Agnieszka Arthur ◽  
Vasilios Panagopoulos ◽  
Amanda J. Page ◽  
...  
Keyword(s):  
Bone Mass ◽  
Glucose Homeostasis ◽  
Female Mice ◽  
Induced Changes

scholarly journals Osteopontin Deficiency Induces Parathyroid Hormone Enhancement of Cortical Bone Formation

Endocrinology ◽  
2003 ◽  
Vol 144 (5) ◽  
pp. 2132-2140 ◽  
Author(s):  
Keiichiro Kitahara ◽  
Muneaki Ishijima ◽  
Susan R. Rittling ◽  
Kunikazu Tsuji ◽  
Hisashi Kurosawa ◽  
...  
Keyword(s):  
Bone Mineral Density ◽  
Bone Formation ◽  
Bone Mass ◽  
Cortical Bone ◽  
Cancellous Bone ◽  
Wild Type ◽  
Mineral Density ◽  
Cortical Bone Mass ◽  
Intermittent Pth

Intermittent PTH treatment increases cancellous bone mass in osteoporosis patients; however, it reveals diverse effects on cortical bone mass. Underlying molecular mechanisms for anabolic PTH actions are largely unknown. Because PTH regulates expression of osteopontin (OPN) in osteoblasts, OPN could be one of the targets of PTH in bone. Therefore, we examined the role of OPN in the PTH actions in bone. Intermittent PTH treatment neither altered whole long-bone bone mineral density nor changed cortical bone mass in wild-type 129 mice, although it enhanced cancellous bone volume as reported previously. In contrast, OPN deficiency induced PTH enhancement of whole-bone bone mineral density as well as cortical bone mass. Strikingly, although PTH suppressed periosteal bone formation rate (BFR) and mineral apposition rate (MAR) in cortical bone in wild type, OPN deficiency induced PTH activation of periosteal BFR and MAR. In cancellous bone, OPN deficiency further enhanced PTH increase in BFR and MAR. Analysis on the cellular bases for these phenomena indicated that OPN deficiency augmented PTH enhancement in the increase in mineralized nodule formation in vitro. OPN deficiency did not alter the levels of PTH enhancement of the excretion of deoxypyridinoline in urine, the osteoclast number in vivo, and tartrate-resistant acid phosphatase-positive cell development in vitro. These observations indicated that OPN deficiency specifically induces PTH activation of periosteal bone formation in the cortical bone envelope.

scholarly journals Mutation of the Galectin-3 Glycan Binding Domain (Lgals3-R200S) Enhances Cortical Bone Expansion in Male and Trabecular Bone Mass in Female Mice

2020 ◽  
Author(s):  
Kevin A. Maupin ◽  
Daniel Dick ◽  
VARI Vivarium ◽  
Transgenics Core ◽  
Bart O. Williams
Keyword(s):  
Bone Mass ◽  
Trabecular Bone ◽  
Cortical Bone ◽  
Mutant Mice ◽  
Slight Variation ◽  
Female Mice ◽  
Bone Phenotype ◽  
Bone Expansion ◽  
Galectin 3 ◽  
Trabecular Bone Mass

AbstractThe study of galectin-3 is complicated by its ability to function both intracellularly and extracellularly. While the mechanism of galectin-3 secretion is unclear, studies have shown that the mutation of a highly conserved arginine to a serine in human galectin-3 (LGALS3-R186S) blocks glycan binding and secretion. To gain insight into the roles of extracellular and intracellular functions of galectin-3, we generated mice with the equivalent mutation (Lgals3-R200S) using CRISPR/Cas9-directed homologous recombination. Consistent with a reduction in galectin-3 secretion, we observed significantly reduced galectin-3 protein levels in the plasma of heterozygous and homozygous mutant mice. We observed a similar increased bone mass phenotype in Lgals3-R200S mutant mice at 36 weeks as we previously observed in Lgals3-KO mice with slight variation. Like Lgals3-KO mice, Lgals3-R200S females, but not males, had significantly increased trabecular bone mass. However, only male Lgals3-R200S mice showed increased cortical bone expansion, which we had previously observed in both male and female Lgals3-KO mice and only in female mice using a separate Lgals3 null allele (Lgals3). These results suggest that the trabecular bone phenotype of Lgals3-KO mice was driven primarily by loss of extracellular galectin-3. However, the cortical bone phenotype of Lgals3-KO mice may have also been influenced by loss of intracellular galectin-3. Future analyses of these mice will aid in identifying the cellular and molecular mechanisms that contribute to the Lgals3-deficient bone phenotype as well as aid in distinguishing the extracellular vs. intracellular roles of galectin-3 in various signaling pathways.

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