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Mechanisms underpinning glucocorticoid impaired chondrogenesis and bone growth

Reference	BBS/E/R/00000682
Principal Investigator / Supervisor	Professor Colin Farquharson
Co-Investigators / Co-Supervisors
Institution	The Roslin Institute
Department	The Roslin Institute Department
Funding type	Research
Value (£)	989,684
Status	Completed
Type	Institute Project
Start date	01/04/2004
End date	31/03/2008
Duration	48 months

Abstract

Retardation of bone growth during embryogenesis in the neonate is a developmental disorder that occurs in animals and man. One of the mechanisms known to be responsible for this disorder is elevated glucocorticoid (GC) steroid levels. It is proposed to identify the GC-dependent gene cascade, which underpins this developmental disorder using the mouse as an experimental model and exploiting state of the art techniques in functional genomics. The hypothesis to be tested is that GC control of chondrocyte proliferation is mediated by the induction of p21, p53 and PTHrP-Ihh signaling pathways and pre-receptor metabolism by 11-beta-HSDs. A mouse cDNA microarray will be used to elucidate the genes regulated by GCs and gene function will be assessed in vitro and in vivo using transgenic mice and siRNA. This strategy will determine the mechanisms by which GCs disrupt key developmental events and signaling pathways during growth plate development.

Summary

unavailable

Committee	Closed Committee - Genes & Developmental Biology (GDB)
Research Topics	X – not assigned to a current Research Topic
Research Priority	X – Research Priority information not available
Research Initiative	X - not in an Initiative
Funding Scheme	X – not Funded via a specific Funding Scheme

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