Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.24.3 (collagenase)
 18,340 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The ability of the anabolic steroid, stanozolol, to stimulate procollagenase production by human synovial and skin fibroblasts was examined in an in vitro assay system. Stanozolol is used therapeutically to treat a variety of connective tissue and vascular disorders and its clinical effects suggest that it can modulate connective tissue breakdown. The results showed that stanozolol was capable, in a dose dependent manner, of significantly stimulating procollagenase production by skin fibroblasts. However, in three synovial fibroblast lines no evidence was found of increased collagenase production following treatment with stanozolol; although the synovial fibroblasts secreted significantly increased amounts of procollagenase in response to IL-1. These results may shed some light on the mechanism of action in vivo of stanozolol in the treatment of connective tissue disorders.
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PMID:The effect of the anabolic steroid, stanozolol, on the production of procollagenase by human synovial and skin fibroblasts in vitro. 255 1

The anabolic steroid stanozolol stimulates the production of prostaglandin E2 (PGE2) and the matrix metalloproteinases collagenase and stromelysin in human skin fibroblasts but not in rheumatoid synovial fibroblasts. The basis for these differential responses was investigated at the levels of DNA synthesis and steroid receptor binding. Stanozolol inhibited fibroblast growth factor (FGF)-stimulated DNA synthesis in both the skin and synovial fibroblasts, showing that both cell types were capable of responding to the compound. Competitive binding assays indicated that stanozolol bound specifically to both the skin and synovial fibroblasts. Binding of stanozolol to both cell types could be partially displaced by progesterone, indicating that stanozolol binds to the progesterone receptor. Immunocytochemical studies confirmed the presence of progesterone receptors on skin and synovial fibroblasts. However, progesterone failed to elicit any response with respect to collagenase production in either cell type. Nortestosterone, dexamethasone and 17 beta-oestradiol had no effect on binding of stanozolol to either cell type. These results indicate that the inhibition of DNA synthesis by stanozolol is elicited through the progesterone receptor. The effects of stanozolol on collagenase and PGE2 production are mediated by a different receptor, present on skin but not synovial fibroblasts, and as yet unidentified.
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PMID:The differential effects of stanozolol on human skin and synovial fibroblasts in vitro: DNA synthesis and receptor binding. 807 19