The DOI matches its Crossref record; 1 of the 1 references it cites were found in a registry or an index.
The Role of Estrogen in the Control of Rat Osteocyte Apoptosis
Abstract
We have previously shown that estrogen withdrawal by gonadotrophin-releasing hormone analogs (GnRHa) induces osteocyte death via apoptosis in human bone. Although it is likely that the increase in osteocyte death via apoptosis was related to the loss of estrogen, these experiments could not rule out a direct role for the GnRHa. Therefore, in this study, we have used a rat model of ovariectomy (OVX) to determine whether the effect of estrogen withdrawal extends to other species and to clarify the role of estrogen in the maintenance of osteocyte viability. Twelve 9-week-old rats were divided into three treatment groups: sham operated (SHAM) (n = 4), OVX (n = 4), and OVX + estrogen (E2) (25 μg/day) (n = 4). At 3 weeks following the start of treatment, tibial bones were removed. The percentage of osteocytes displaying DNA breaks, using an in situ nick-translation method, was significantly higher in the OVX group compared with the SHAM control in both cortical bone (10.04% vs. 2.31%, respectively; p < 0.0001) and trabecular bone (6.44% vs. 1.58%, respectively; p = 0.003). Addition of estrogen in the OVX animals completely abrogated the increase in osteocyte apoptosis in cortical bone (0.78%) and trabecular bone (1.17%). The percentage of apoptotic osteocytes decreased with increasing distance from the primary/secondary spongiosa interface below the growth plate in the OVX model and the OVX + E2 model. Nuclear morphology and electrophoresis of DNA confirmed the presence of apoptotic cells in the samples. In conclusion, OVX in the rat results in an increase in osteocyte apoptosis as a direct or indirect result of E2 loss. Addition of estrogen in the OVX animals prevents this increase in osteocyte apoptosis. These data confirm an important role for estrogen in the control of osteocyte apoptosis and the maintenance of osteocyte viability. Estrogen deficiency might, through compromising the viability of osteocyte networks, reduce the ability of bone to respond appropriately to loading.
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Citations
Cites
Estrogen promotes apoptosis of murine osteoclasts mediated by TGF–β
Hughes, D. E., Dai, A., Tiffee, J. C., Li, H. H., Mundy, G. R., & Boyce, B. F. (1996) · Nature Medicine · doi:10.1038/nm1096-1132 · Cited by 813 · cited 1×
“For example, it stimulates apoptosis in osteoclasts((30)) and inhibits apoptosis in nerve cells,((31,32)) endothelial cells,((33)) and some epithelial cells.”
Background
Cited by
Sex Steroids and the Construction and Conservation of the Adult Skeleton
Riggs, B. L., Khosla, S., & Melton, L. J. (2002) · Endocrine Reviews · doi:10.1210/edrv.23.3.0465 · Cited by 1,846
Estrogen deficiency and bone loss: an inflammatory tale
Weitzmann, M. N. (2006) · Journal of Clinical Investigation · doi:10.1172/jci28550 · Cited by 990
Khosla, S., Oursler, M. J., & Monroe, D. G. (2012) · Trends in Endocrinology & Metabolism · doi:10.1016/j.tem.2012.03.008 · Cited by 943
Estrogens and androgens in skeletal physiology and pathophysiology
Almeida, M., Laurent, M. R., Dubois, V., Claessens, F., O'Brien, C. A., Bouillon, R., Vanderschueren, D., & Manolagas, S. C. (2017) · Physiological Reviews · doi:10.1152/physrev.00033.2015 · Cited by 860
Verborgt, O., Gibson, G. J., & Schaffler, M. B. (2000) · Journal of Bone and Mineral Research · doi:10.1359/jbmr.2000.15.1.60 · Cited by 731
Metadata
- Authors
- Tomkinson, A., Gevers, E. F., Wit, J. M., Reeve, J., & Noble, B. S.
- Venue
- Journal of Bone and Mineral Research
- Publisher
- Oxford University Press (OUP)
- Published
- 1998-08-01
- Volume
- 13
- Issue
- 8
- Pages
- 1243-1250
- ISSN
- 0884-0431 (ISSN-L)
- 1523-4681
- OpenAlex
- W2008698339
- Cited by
- 302
- References
- 1
- FWCI
- 6.45
- Type
- journal article
- Language
- en
- Open access
- closed
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- Tomkinson, A., Gevers, E. F., Wit, J. M., Reeve, J., & Noble, B. S. (1998). The Role of Estrogen in the Control of Rat Osteocyte Apoptosis. Journal of Bone and Mineral Research. https://doi.org/10.1359/jbmr.1998.13.8.1243
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
