Exposure to chronic stress induces bone loss via glucocorticoid signalling in osteoblasts

2016 ◽  
Author(s):  
Holger Henneicke ◽  
Jing-Bao Li ◽  
Sylvia J Gasparini ◽  
Markus J Seibel ◽  
Hong Zhou
Keyword(s):  
Bone Loss ◽  
Chronic Stress

scholarly journals Chronic Mild Stress Causes Bone Loss via an Osteoblast-Specific Glucocorticoid-Dependent Mechanism

Endocrinology ◽  
2017 ◽  
Vol 158 (6) ◽  
pp. 1939-1950 ◽  
Author(s):  
Holger Henneicke ◽  
Jingbao Li ◽  
Sarah Kim ◽  
Sylvia J. Gasparini ◽  
Markus J. Seibel ◽  
...  
Keyword(s):  
Bone Loss ◽  
Chronic Stress ◽  
Structural Parameters ◽  
Chronic Mild Stress ◽  
Bone Resorption Marker ◽  
Mild Stress ◽  
Male Mice ◽  
Female Mice ◽  
Glucocorticoid Signaling ◽  
The Impact

Abstract Chronic stress and depression are associated with alterations in the hypothalamic–pituitary–adrenal signaling cascade and considered a risk factor for bone loss and fractures. However, the mechanisms underlying the association between stress and poor bone health are unclear. Using a transgenic (tg) mouse model in which glucocorticoid signaling is selectively disrupted in mature osteoblasts and osteocytes [11β-hydroxysteroid-dehydrogenase type 2 (HSD2)OB-tg mice], the present study examines the impact of chronic stress on skeletal metabolism and structure. Eight-week-old male and female HSD2OB-tg mice and their wild-type (WT) littermates were exposed to chronic mild stress (CMS) for the duration of 4 weeks. At the endpoint, L3 vertebrae and tibiae were analyzed by micro–computed tomography and histomorphometry, and bone turnover was measured biochemically. Compared with nonstressed controls, exposure to CMS caused an approximately threefold increase in serum corticosterone concentrations in WT and HSD2OB-tg mice of both genders. Compared with controls, CMS resulted in loss of vertebral trabecular bone mass in male WT mice but not in male HSD2OB-tg littermates. Furthermore, both tibial cortical area and area fraction were reduced in stressed WT but not in stressed HSD2OB-tg male mice. Osteoclast activity and bone resorption marker were increased in WT males following CMS, features absent in HSD2OB-tg males. Interestingly, CMS had little effect on vertebral and long-bone structural parameters in female mice. We conclude that in male mice, bone loss during CMS is mediated via enhanced glucocorticoid signaling in osteoblasts (and osteocytes) and subsequent activation of osteoclasts. Female mice appear resistant to the skeletal effects of CMS.

Exposure to chronic stress induces bone loss via glucocorticoid signalling in osteoblasts

2016 ◽  
Author(s):  
Holger Henneicke ◽  
Jing-Bao Li ◽  
Sylvia J Gasparini ◽  
Markus J Seibel ◽  
Hong Zhou
Keyword(s):  
Bone Loss ◽  
Chronic Stress

scholarly journals Astrocytes in the Ventromedial Hypothalamus Involve Chronic Stress-Induced Anxiety and Bone Loss in Mice

2021 ◽  
Vol 2021 ◽  
pp. 1-16
Author(s):  
Yunhui Liu ◽  
Jie Shao ◽  
Dashuang Gao ◽  
Lu Zhang ◽  
Fan Yang
Keyword(s):  
Bone Loss ◽  
Chronic Stress ◽  
Neural Circuits ◽  
Cell Function ◽  
Ventromedial Hypothalamus ◽  
Brain Regions ◽  
Receptor Blocker ◽  
Steroidogenic Factor 1 ◽  
Regulation Of Metabolism ◽  
Nmda Receptor Blocker

Chronic stress is one of the main risk factors of bone loss. While the neurons and neural circuits of the ventromedial hypothalamus (VMH) mediate bone loss induced by chronic stress, the detailed intrinsic mechanisms within the VMH nucleus still need to be explored. Astrocytes in brain regions play important roles in the regulation of metabolism and anxiety-like behavior through interactions with surrounding neurons. However, whether astrocytes in the VMH affect neuronal activity and therefore regulate chronic stress-induced anxiety and bone loss remain elusive. In this study, we found that VMH astrocytes were activated during chronic stress-induced anxiety and bone loss. Pharmacogenetic activation of the Gi and Gq pathways in VMH astrocytes reduced and increased the levels of anxiety and bone loss, respectively. Furthermore, activation of VMH astrocytes by optogenetics induced depolarization in neighboring steroidogenic factor-1 (SF-1) neurons, which was diminished by administration of N-methyl-D-aspartic acid (NMDA) receptor blocker but not by alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor blocker. These results suggest that there may be a functional “glial-neuron microcircuit” in VMH nuclei that mediates anxiety and bone loss induced by chronic stress. This study not only advances our understanding of glial cell function but also provides a potential intervention target for chronic stress-induced anxiety and bone loss therapy.

scholarly journals Effects of Active Mastication on Chronic Stress-Induced Bone Loss in Mice

2015 ◽  
Vol 12 (12) ◽  
pp. 952-957 ◽  
Author(s):  
Kagaku Azuma ◽  
Manabu Furuzawa ◽  
Shu Fujiwara ◽  
Kumiko Yamada ◽  
Kin-ya Kubo
Keyword(s):  
Bone Loss ◽  
Chronic Stress

The influence of chronic stress imposed on pregnant rats on the induced bone loss in their adult offspring

2012 ◽  
Vol 57 (5) ◽  
pp. 477-482 ◽  
Author(s):  
Alex Semenoff-Segundo ◽  
Tereza Aparecida Delle Vedove Semenoff ◽  
Álvaro Henrique Borges ◽  
Fábio Luiz Miranda Pedro ◽  
Leonardo Stephan Caporossi ◽  
...  
Keyword(s):  
Bone Loss ◽  
Chronic Stress ◽  
Adult Offspring ◽  
Pregnant Rats

scholarly journals A GABAergic neural circuit in the ventromedial hypothalamus mediates chronic stress–induced bone loss

2020 ◽  
Vol 130 (12) ◽  
pp. 6539-6554
Author(s):  
Fan Yang ◽  
Yunhui Liu ◽  
Shanping Chen ◽  
Zhongquan Dai ◽  
Dazhi Yang ◽  
...  
Keyword(s):  
Bone Loss ◽  
Chronic Stress ◽  
Neural Circuit ◽  
Ventromedial Hypothalamus

Bone loss in patients with Crohn's disease: A longterm-follow up study

2001 ◽  
Vol 120 (5) ◽  
pp. A628-A628
Author(s):  
P CLEMENS ◽  
V HAWIG ◽  
M MUELLER ◽  
J SCAENZLIN ◽  
B KLUMP ◽  
...  
Keyword(s):  
Crohn’S Disease ◽  
Crohn's Disease ◽  
Bone Loss ◽  
Follow Up Study

OC Helps Anorexic Teenagers Offset Bone Loss

2005 ◽  
Vol 39 (8) ◽  
pp. 36
Author(s):  
JANE SALODOF MACNEIL
Keyword(s):  
Bone Loss
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