The DOI matches its Crossref record; 6 of the 6 references it cites were found in a registry or an index.
Promotion of osteoclast survival and antagonism of bisphosphonate-induced osteoclast apoptosis by glucocorticoids
Open accessAbstract
Glucocorticoids depress bone formation by inhibiting osteoblastogenesis and increasing osteoblast apoptosis. However, the role of bone resorption in the initial rapid phase of bone loss characteristic of glucocorticoid-induced osteoporosis is unexplained, and the reason for the efficacy of bisphosphonates in this condition remains unknown. We report that in murine osteoclast cultures, glucocorticoids prolonged the baseline survival of osteoclasts and antagonized bisphosphonate-induced caspase activation and apoptosis by a glucocorticoid receptor–mediated action. Consistent with the in vitro evidence, in a murine model of glucocorticoid-induced osteoporosis, the number of cancellous osteoclasts increased, even though osteoclast progenitor number was reduced. Moreover, in mice receiving both glucocorticoids and bisphosphonates, the expected proapoptotic effect of bisphosphonates on osteoclasts was abrogated, as evidenced by maintenance of osteoclast numbers and, additionally, loss of bone density. In contrast, bisphosphonate administration prevented glucocorticoid-induced osteoblast apoptosis. These results indicate that the early loss of bone with glucocorticoid excess is caused by extension of the life span of pre-existing osteoclasts, an effect not preventable by bisphosphonates. Therefore, the early beneficial effects of these agents must be due, in part, to prolonging the life span of osteoblasts.
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Cites
Weinstein, R. S., Jilka, R. L., Parfitt, A. M., & Manolagas, S. C. (1998) · Journal of Clinical Investigation · doi:10.1172/jci2799 · Cited by 1,753 · cited 7×
“We have reported previously that glucocorticoid administration to mice for 27 days (a period representing chronic rather than short-term drug exposure) decreases the number of osteoblast and osteoclast progenitors, decreases the cancellous osteoblast and osteoclast perimeters, and increases osteoblast apoptosis (20).”
InfluentialSelf-citationAlendronate for the Prevention and Treatment of Glucocorticoid-Induced Osteoporosis
Saag, K. G., Emkey, R., Schnitzer, T. J., Brown, J. P., Hawkins, F., Goemaere, S., Thamsborg, G., Liberman, U. A., Delmas, P. D., Malice, M.-P., et al. (1998) · New England Journal of Medicine · doi:10.1056/nejm199807303390502 · Cited by 1,258
Prevention of osteocyte and osteoblast apoptosis by bisphosphonates and calcitonin
Plotkin, L. I., Weinstein, R. S., Parfitt, A. M., Roberson, P. K., Manolagas, S. C., & Bellido, T. (1999) · Journal of Clinical Investigation · doi:10.1172/jci6800 · Cited by 890 · cited 2×
“Despite the uncertainty about the role of bone resorption in the pathogenesis of osteoporosis induced by long-term glucocorticoid administration, the benefits of bisphosphonate therapy in this disorder have been ascribed solely to antiresorptive effects and preservation of, or increases in, bone density (13, 16, 17),…”
Self-citationEstrogen promotes apoptosis of murine osteoclasts mediated by TGF–β
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Carbonare, L. D., Arlot, M. E., Chavassieux, P. M., Roux, J. P., Portero, N. R., & Meunier, P. J. (2001) · Journal of Bone and Mineral Research · doi:10.1359/jbmr.2001.16.1.97 · Cited by 309
Weinstein, R. S., Jilka, R. L., Parfitt, A. M., & Manolagas, S. C. (1997) · Endocrinology · doi:10.1210/endo.138.9.5359 · Cited by 126
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Cited by
Matrix-embedded cells control osteoclast formation
Xiong, J., Onal, M., Jilka, R. L., Weinstein, R. S., Manolagas, S. C., & O'Brien, C. A. (2011) · Nature Medicine · doi:10.1038/nm.2448 · Cited by 1,304
Self-citationAguirre, J. I., Plotkin, L. I., Stewart, S. A., Weinstein, R. S., Parfitt, A. M., Manolagas, S. C., & Bellido, T. (2006) · Journal of Bone and Mineral Research · doi:10.1359/jbmr.060107 · Cited by 494
Self-citationGlucocorticoids Act Directly on Osteoclasts to Increase Their Life Span and Reduce Bone Density
Jia, D., O’Brien, C. A., Stewart, S. A., Manolagas, S. C., & Weinstein, R. S. (2006) · Endocrinology · doi:10.1210/en.2006-0459 · Cited by 394
Self-citationGiant Osteoclast Formation and Long-Term Oral Bisphosphonate Therapy
Weinstein, R. S., Roberson, P. K., & Manolagas, S. C. (2009) · New England Journal of Medicine · doi:10.1056/nejmoa0802633 · Cited by 391
Self-citationBisphosphonates: An Update on Mechanisms of Action and How These Relate to Clinical Efficacy
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Metadata
- Authors
- Weinstein, R. S., Chen, J.-R., Powers, C. C., Stewart, S. A., Landes, R. D., Bellido, T., Jilka, R. L., Parfitt, A. M., & Manolagas, S. C.
- Venue
- Journal of Clinical Investigation
- Published
- 2002-04-15
- Volume
- 109
- Issue
- 8
- Pages
- 1041-1048
- ISSN
- 0021-9738 (ISSN-L)
- OpenAlex
- W4240799970
- Cited by
- 313
- References
- 6
- FWCI
- 5.94
- Type
- journal article
- Language
- en
- Open access
- bronze
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