Glucocorticoid dose determines osteocyte cell fate
Open accessAbstract
In response to cellular insult, several pathways can be activated, including necrosis, apoptosis, and autophagy. Because glucocorticoids (GCs) have been shown to induce both osteocyte apoptosis and autophagy, we sought to determine whether osteocyte cell fate in the presence of GCs was dose dependent by performing in vivo and in vitro studies. Male Swiss-Webster mice were treated with slow-release prednisolone pellets at 1.4, 2.8, and 5.6 mg/kg/d for 28 d. An osteocyte cell line, MLO-Y4 cells, was treated with various doses of dexamethasone. We found that GC treatments dose dependently decreased activation of antioxidant-, autophagy-, and antiapoptosis-focused RT-PCR gene pathways in mouse cortical bone. The activation of antioxidant genes was correlated with autophagy gene expression after the GC treatments. The presence of osteocyte autophagy, as detected by immunostaining for LC3, increased ∼50% at the distal femur cortical bone region but not at trabecular bone region at the 1.4 and 2.8 mg/kg/d GC dose levels. The number of apoptotic osteocytes was increased at the cortical bone region by ∼40% initially observed at the 2.8 mg/kg/d dose level. In addition, the presence of the osteocyte autophagy was associated with an increased protein level of cathepsin K in vitro after the GC treatments. In summary, we found that GC treatment dose-dependently decreased antioxidant gene expression, with lower GC doses activating autophagy, whereas a higher dose increased apoptosis. These data suggest that autophagy may provide a mechanism for osteocytes to survive the stress after GC exposure and provide further insight into how GCs alter bone cell fate.
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Osteocyte autophagy is crucial to the regulation of bone structure and plays a role in glucocorticoid-induced bone fragility.
“We have reported that osteocyte autophagy is crucial to the regulation of bone structure and plays a role in GC induced bone fragility [44, 68].”
From Prevention of glucocorticoid induced bone changes with beta-ecdysone (2015) · cites this paper as [44]
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- Authors
- Jia, J., Yao, W., Guan, M., Dai, W., Shahnazari, M., Kar, R., Bonewald, L., Jiang, J. X., & Lane, N. E.
- Affiliations
- University of California Davis Medical Center (US)
- The University of Texas at San Antonio Health Science Center (US)
- University of Missouri–Kansas City (US)
- Corresponding author
- Lane, Nancy E.
- Venue
- The FASEB Journal
- Publisher
- Wiley
- Published
- 2011-06-24
- Volume
- 25
- Issue
- 10
- Pages
- 3366-3376
- ISSN
- 0892-6638 (ISSN-L)
- 1530-6860
- PMC
- PMC3177583
- OpenAlex
- W2156576798
- Cited by
- 157
- References
- 81
- Citations by year
- 2026: 5 · 2025: 4 · 2024: 6 · 2023: 7 · 2022: 12 · 2021: 12 · 2020: 15 · 2019: 18 · 2018: 18 · 2017: 8 · 2016: 8 · 2015: 9 · 2014: 12 · 2013: 15 · 2012: 8
- FWCI
- 4.55
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- The FASEB Journal (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (1K12-HD05195801)
- National Institute of Child Health and Human Development (R01-AR043052-07)
- Office of Research on Women's Health (K24-AR048841)
- Office of Dietary Supplements (5R21-AR57515-2)
- Welch Foundation (AQ-1507)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Bone Metabolism and Diseases
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Health Sciences › Medicine › Orthopedics and Sports Medicine › Bone health and osteoporosis research
- Keywords
- glucocorticoids, osteocytes, cell fate, dose dependence, autophagy, apoptosis, antioxidant gene expression, dexamethasone, prednisolone, MLO-Y4 cells, cortical bone, trabecular bone, cathepsin K, LC3
- MeSH terms
- Animals, Autophagy, Cell Line, Delayed-Action Preparations, Dexamethasone, Dose-Response Relationship, Drug, Glucocorticoids, Male, Osteocytes, Prednisolone, Apoptosis, Mice, Cathepsin K
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