Genetic approaches to determine the role of glucocorticoid signaling in osteoblasts |
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Authors: | Harrison John R Woitge Henning W Kream Barbara E |
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Institution: | (1) Department of Orthodontics, School of Dental Medicine, USA;(2) School of Medicine, University of Connecticut Health Center, Farmington, CT |
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Abstract: | A variety of in vivo and in vitro experimental models have been used to explore the effects of glucococorticoids in bone.
Chronically high levels of glucocorticoids typically decrease bone mass in humans and animals and inhibit markers of bone
formation in organ and cell cultures. However, under certain experimental conditions, glucocorticoids can stimulate osteoblast
differentiation and bone formation in vitro. The relevance of these effects seen in culture models to the role of endogenous
glucocorticoids in bone remains unclear. In this article, we briefly review possible pathways for the opposing effects of
glucocorticoids on bone formation and propose several genetic loss-of-function mouse models in which disruption of glucocorticoid
signaling in cells of the osteoblast lineage would provide a means to determine the role of endogenous glucocorticoids in
bone. |
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Keywords: | Glucocorticoids bone osteoblast Cre/loxP recombination 11β -hydroxysteroid dehydrogenase transgenesis |
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