pubmed-article:17603917 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:17603917 | lifeskim:mentions | umls-concept:C0005939 | lld:lifeskim |
pubmed-article:17603917 | lifeskim:mentions | umls-concept:C0225369 | lld:lifeskim |
pubmed-article:17603917 | lifeskim:mentions | umls-concept:C0682564 | lld:lifeskim |
pubmed-article:17603917 | lifeskim:mentions | umls-concept:C0017710 | lld:lifeskim |
pubmed-article:17603917 | lifeskim:mentions | umls-concept:C1710082 | lld:lifeskim |
pubmed-article:17603917 | lifeskim:mentions | umls-concept:C1513400 | lld:lifeskim |
pubmed-article:17603917 | lifeskim:mentions | umls-concept:C0205225 | lld:lifeskim |
pubmed-article:17603917 | lifeskim:mentions | umls-concept:C1521840 | lld:lifeskim |
pubmed-article:17603917 | pubmed:dateCreated | 2007-7-30 | lld:pubmed |
pubmed-article:17603917 | pubmed:abstractText | Glucocorticoids (GCs) are widely used anti-inflammatory drugs. While useful in clinical practice, patients taking GCs often suffer from skeletal side effects including growth retardation in children and adolescents, and decreased bone quality in adults. On a physiological level, GCs have been implicated in the regulation of chondrogenesis and osteoblast differentiation, as well as maintaining homeostasis in cartilage and bone. We identified the glucocorticoid receptor (GR) as a potential regulator of chondrocyte hypertrophy in a microarray screen of primary limb bud mesenchyme micromass cultures. Some targets of GC regulation in chondrogenesis are known, but the global effects of pharmacological GC doses on chondrocyte gene expression have not been comprehensively evaluated. | lld:pubmed |
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