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

A method was developed for the determination of urinary chondroitin sulphate (CS), including dermatan sulphate and chondroitin 4 and 6-sulphates, using an enzymatic degradation with chondroitinase-ABC followed by precipitation with Alcian blue, whereby CS was determined as the difference between undigested and chondroitinase digested material. The method was linear in the range 0-100 mg l-1 with a detection limit of 1 mg l-1 and allowed determinations on small urine volumes without pretreatment of the urine. It could be demonstrated that males excreted more CS than females, and growing children had the highest urinary content of CS. Renal calcium stone formers did not differ from healthy controls in urinary CS. Patients with acromegaly had a higher excretion of CS compared with controls. There was also, in these patients, a positive correlation between the serum growth hormone levels and the urinary CS, indicating that CS-excretion may be an estimate of the activity of the pituitary disorder.
 ...
PMID:Enzymatic determination of urinary chondroitin sulphate: applications in renal stone disease and acromegaly. 242 21

Partial-thickness defects evolving in mature articular cartilage do not heal spontaneously. This type of defect was created in the articular cartilage of adult rabbits and Yucatan minipigs, and the effects of chondroitinase ABC or trypsin, fibrin clots, and mitogenic growth factors on the healing process were examined histologically at intervals ranging from one to forty-eight weeks. The effect of chondroitinase ABC or trypsin was examined initially. Articular cartilage contains macromolecules, including proteoglycans, which render the surfaces of this tissue, and of partial-thickness defects within it, antiadhesive. Chondroitinase ABC digests the glycosaminoglycan chains of cartilage proteoglycans, and trypsin degrades their core proteins. To test the hypothesis that mesenchymal cells may be prevented from adhering to and migrating over the surfaces of partial-thickness defects by proteoglycans, we removed a superficial layer of these macromolecules from the surface of the defect with use of one of these enzymes. The treatment evoked an increase in the coverage of the defect surface with mesenchymal cells; when combined with the local application of a mitogenic growth factor (basic fibroblast growth factor, transforming growth factor-beta 1, epidermal growth factor, insulin-like growth factor-1, or growth hormone), the coverage was more extensive but mesenchymal cells did not extend into and completely fill the volume of the defect. When the surface of the defect was treated with chondroitinase ABC and the cavity of the defect was filled with a fibrin clot to furnish a matrix or scaffolding for the migration of cells therein, there was migration and proliferation of cells throughout the volume of the defect but at a low population density. Mesenchymal cells remodeled the deposited fibrin matrix, which was replaced by a loose fibrous connective tissue. When defects that had been treated with chondroitinase ABC were filled with a fibrin clot containing a mitogenic growth factor, mesenchymal cells filled the entire cavity of the defect, and the density of the cells was greatly increased, particularly when transforming growth factor-beta 1 was used. Histological studies revealed a continuous layer of mesenchymal cells extending from the synovial membrane across the superficial tangential zone of normal articular cartilage into the defect, indicating that the cells that were recruited for the repair process were of synovial origin. At forty-eight weeks, the entire cavity of the defect remained filled with a fibrous connective tissue.
 ...
PMID:Repair of partial-thickness defects in articular cartilage: cell recruitment from the synovial membrane. 864 29