Journal
JOURNAL OF BONE AND MINERAL RESEARCH
Volume 25, Issue 11, Pages 2479-2488Publisher
WILEY
DOI: 10.1002/jbmr.160
Keywords
GLUCOCORTICOID; OSTEOCYTE; AUTOPHAGY; VIABILITY
Categories
Funding
- National Institutes of Health (NIH) [PO1 AR46798, R01 AR043052, K24 AR04884, K12 HD05195801]
- Welch Foundation [AQ-1507]
- University of California at Davis
- Endowed Chair for Aging at the University of California at Davis
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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 alpha (TNF alpha) 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 (C) 2010 American Society for Bone and Mineral Research
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