CORE
🇺🇦
make metadata, not war
Services
Services overview
Explore all CORE services
Access to raw data
API
Dataset
FastSync
Content discovery
Recommender
Discovery
OAI identifiers
OAI Resolver
Managing content
Dashboard
Bespoke contracts
Consultancy services
Support us
Support us
Membership
Sponsorship
Community governance
Advisory Board
Board of supporters
Research network
About
About us
Our mission
Team
Blog
FAQs
Contact us
Glucocorticoid-Induced Autophagy in Osteocytes
Authors
Sondip K Biswas
Lynda F Bonewald
+7 more
Jelica Gluhak-Heinrich
Jean X Jiang
Rekha Kar
Nancy E Lane
Woo-Kuen Lo
Xuechun Xia
Wei Yao
Publication date
1 November 2010
Publisher
Wiley Subscription Services, Inc., A Wiley Company
View
on
PubMed
Abstract
Glucocorticoid (GC) therapy is the most frequent cause of secondary osteoporosis. In this study we have demonstrated that GC treatment induced the development of autophagy, preserving osteocyte viability. GC treatment resulted in an increase in autophagy markers and the accumulation of autophagosome vacuoles in vitro and in vivo promoted the onset of the osteocyte autophagy, as determined by expression of autophagy markers in an animal model of GC-induced osteoporosis. An autophagy inhibitor reversed the protective effects of GCs. The effects of GCs on osteocytes were in contrast to tumor necrosis factor α (TNF-α), which induced apoptosis but not autophagy. Together this study reveals a novel mechanism for the effect of GC on osteocytes, shedding new insight into mechanisms responsible for bone loss in patients receiving GC therapy. © 2010 American Society for Bone and Mineral Research
Similar works
Full text
Open in the Core reader
Download PDF
Available Versions
Sustaining member
eScholarship - University of California
See this paper in CORE
Go to the repository landing page
Download from data provider
oai:escholarship.org:ark:/1303...
Last time updated on 25/12/2021