The DOI matches its Crossref record; 75 of the 75 references it cites were found in a registry or an index.
Glucocorticoids and Tumor Necrosis Factor α Increase Oxidative Stress and Suppress Wnt Protein Signaling in Osteoblasts
Open accessAbstract
Endogenous glucocorticoids (GCs) and inflammatory cytokines contribute to the age-associated loss of bone mass and strength, but the molecular mechanisms responsible for their deleterious effects on the aging skeleton are unclear. Based on evidence that oxidative stress is a causal mechanism of the insulin resistance produced by either one of these two agents, we tested the hypothesis that their adverse skeletal effects also result from increased oxidative stress. We report that administration of prednisolone to mice increased reactive oxygen species (ROS) and the phosphorylation of p66(shc) (an amplifier of H(2)O(2) generation in mitochondria) in bone. Dexamethasone (Dex) and TNFα had a similar effect on osteoblastic cells in vitro. The generation of ROS by Dex and TNFα required PKCβ/p66(shc) signaling and was responsible for the activation of JNK and induction of apoptosis by both agents. The activity of Forkhead box O (FoxO) transcription factors was also increased in response to ROS; however, FoxO activation opposed apoptosis induced by Dex and TNFα. In addition, both agents suppressed Akt phosphorylation as well as Wnt-induced proliferation and osteoblast differentiation. However, the inhibitory actions on Wnt signaling were independent of PKCβ/p66(shc). Instead, they were mediated by inhibition of Akt and stimulation of FoxOs. These results demonstrate that ROS-induced activation of a PKCβ/p66(shc)/JNK signaling cascade is responsible for the pro-apoptotic effects of Dex and TNFα on osteoblastic cells. Moreover, modulation of Akt and FoxOs by GCs and TNFα are cell-autonomous mechanisms of Wnt/β-catenin antagonism contributing to the adverse effects of GC excess and inflammatory cytokines on bone alike.
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Cites
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Weinstein, R. S. (2012) · Endocrinology and Metabolism Clinics of North America · doi:10.1016/j.ecl.2012.04.004 · Cited by 364
Self-citationThe regulation of muscle mass by endogenous glucocorticoids
Braun, T. P., & Marks, D. L. (2015) · Frontiers in Physiology · doi:10.3389/fphys.2015.00012 · Cited by 273
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Hardy, R. S., Zhou, H., Seibel, M. J., & Cooper, M. S. (2018) · Endocrine Reviews · doi:10.1210/er.2018-00097 · Cited by 258
Involvement of the gut microbiota and barrier function in glucocorticoid-induced osteoporosis
Schepper, J. D., Collins, F., Rios-Arce, N. D., Kang, H. J., Schaefer, L., Gardinier, J. D., Raghuvanshi, R., Quinn, R. A., Britton, R., Parameswaran, N., et al. (2020) · Journal of Bone and Mineral Research · doi:10.1002/jbmr.3947 · Cited by 199
Metadata
- Authors
- Almeida, M., Han, L., Ambrogini, E., Weinstein, R. S., & Manolagas, S. C.
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 2011-12
- Volume
- 286
- Issue
- 52
- Pages
- 44326-44335
- ISSN
- 0021-9258 (ISSN-L)
- OpenAlex
- W1981465641
- Cited by
- 270
- References
- 75
- FWCI
- 5.53
- Type
- journal article
- Language
- en
- Open access
- hybrid
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- CoChat. (2026). Citation check: Glucocorticoids and Tumor Necrosis Factor α Increase Oxidative Stress and Suppress Wnt Protein Signaling in Osteoblasts. https://app.cochat.ai/papers/10.1074/jbc.m111.283481
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- Almeida, M., Han, L., Ambrogini, E., Weinstein, R. S., & Manolagas, S. C. (2011). Glucocorticoids and Tumor Necrosis Factor α Increase Oxidative Stress and Suppress Wnt Protein Signaling in Osteoblasts. Journal of Biological Chemistry. https://doi.org/10.1074/jbc.m111.283481
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