Biologically, it has been implicated in the generation of the immune repertoire and the regulation of immune responses,1, 2, 3 and clinically it has been exploited in the therapy of lymphoid malignancies.4 In this review, we summarize current concepts regarding the molecular mechanism of this GC response and resistance against it, and discuss the potential clinical impact of emerging knowledge in this field. Space limitations precluded a complete reference to the large body of literature and we apologize to our colleagues for often citing reviews and exemplary work rather than all relevant original publications.cheap Air Jordans To put our topic into perspective, we first provide a short introduction to the multitude of GC effects and their basic mechanism of action, and briefly discuss distinct forms of cell death as they relate to the topic of this review.
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This suggests that the contrasting anabolic and catabolic effects of glucocorticoids on bone are, at least in part, mediated through the regulation of Wnt expression and its inhibitors in mature osteoblasts. Further evidence for this mechanism has been derived from in vivo studies examining cranial bone development (38).Endogenous glucocorticoids are important in cranial bone development in vivoNeonatal Col2.3 HSD2 transgenic mice exhibit a distinct phenotype characterised by hypoplasia and osteopenia of the cranial skeleton, increased suture patency, ectopic differentiation of cartilage in the sagittal suture and an increased amount of parietal cartilage (38,53). Another mouse model in which the 11HSD2 transgene is expressed in the osteoblast lineage from pre osteoblasts onwards using a 3.6 kb collagen type I (Col3.6) promoter (Col3.6 11HSD2 transgenic) showed a very similar phenotype to the Col2.3 11HSD2 transgenic mice (34).
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