Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.2.1.36 (hyaluronidase)
 4,606 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In 1962, when the immune complex in nephritic glomerular basement membrane (GBM) was clarified as being a type of GBM thickening, Amon and Gayer reported a different type of thickening in the rabbit administered hyaluronidase (an enzyme to degrade hyaluronic acid) and named it 'herniation' of the GBM. As we have been interested for a long time in the disappearance of normally present nonsulfated AMPS, presumably hyaluronic acid (HA), from the glomeruli in humans and experimental animals with chronic glomerulonephritis, we wanted to observe the activity of the enzyme in these conditions. Since a suitable histochemical method for the precise evaluation of hyaluronidase is unavailable, we instead chose beta-glucuronidase(beta-Gase), which is also an enzyme which degrades HA. The principal study was performed by means of light- and electron-microscopic histochemistry of chronic glomerulonephritis produced experimentally in rats and compared the obtained results to those in human chronic glomerulonephritis. The high activity of beta-Gase with a coincidental decrease of AMPS in the glomeruli was observed both in experimental and human chronic glomerulonephritis. The herniation type GBM thickening in the rat was coincidental with the enzyme localization with the disappearance of AMPS from foot processes of epithelial cells overlaying the lesion. The results might suggest the key role of beta-Gase in the deformation of GBM in chronic glomerulonephritis in general.
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PMID:Acid mucopolysaccharide and one of its glomerular degrading enzymes beta-glucuronidase in experimental and human glomerulonephritis. 617 21