Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.6.4 (chondroitinase)
 2,039 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of IL-1 on proteoglycan synthesis was studied after intraarticular injection of IL-1 into the knee joints of rats. IL-1 reduced the sulfated glycosaminoglycan synthesis in the articular cartilage of rats in a dose-dependent fashion. Analysis of the sulfated molecules by chondroitinase ABC digestion followed by composite agarose/acrylamide gel electrophoresis confirmed the proteoglycan nature of the molecules. Immunoprecipitation of the methionine-labeled extracts with a polyclonal antibody against the core protein indicated that the reduction in glycosaminoglycan synthesis was due to an inhibition of the core protein synthesis after IL-1 treatment. IL-1 induced inhibition occurred in both young and old rats and was independent of the prostaglandin pathway, as non-steroidal anti-inflammatory drugs failed to block the inhibition of proteoglycan synthesis by IL-1. The cartilage of rats injected with IL-1 was able to recover with time and synthesize normal amounts of total proteoglycan. However, administration of successive doses resulted in a much delayed return to normal synthesis. These results suggest that IL-1, if available locally in a cyclical fashion, could significantly interfere with the ability of cartilage to repair by causing a prolonged suppression of proteoglycan synthesis.
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PMID:Intra-articular administration of interleukin-1 causes prolonged suppression of cartilage proteoglycan synthesis in rats. 156 Jul 85

Accumulation of glomerular extracellular matrix is a prominent feature of most forms of progressive glomerular disease. Since some growth factors may play a role in extracellular matrix production, we examined the effects of transforming growth factor-beta (TGF-beta), interleukin 1, platelet derived growth factor, and tumor necrosis factor on the production of extracellular matrix components by cultured rat mesangial cells. In control experiments we found that mesangial cells produced two distinct proteoglycans identified as the small chondroitin/dermatan sulfate proteoglycans biglycan (PG I) and decorin (PG II) by showing that their mobility on SDS-PAGE changed upon digestion by chondroitinase ABC, and that they reacted with antibodies raised against synthetic peptides from the core protein sequence of human biglycan and decorin. Exposure to TGF-beta for 48 hours stimulated an 8- to 10-fold increase in the biglycan and decorin bands, and induced a structural change detected as a shift in electrophoretic mobility. TGF-beta did not demonstrably affect the production of other matrix proteins by the mesangial cells. The other growth factors tested had no comparable effect on the production of proteoglycans or other extracellular matrix components by these cells. Our results show that TGF-beta is unique among growth factors in its regulatory effects on mesangial cell proteoglycan production. The release or activation of TGF-beta during glomerular injury could mediate the accumulation of proteoglycans in the extracellular matrix and predispose the kidney to development of glomerulosclerosis.
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PMID:Transforming growth factor-beta regulates production of proteoglycans by mesangial cells. 240 84