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)

Corneas from mouse, rat and rabbit were analysed quantitatively and/or qualitatively for collagen and acid glycosaminoglycans. They were examined by light and electron microscopy, using Alcian blue and Cupromeronic blue, in critical electrolyte concentration methods, with or without digestion by hyaluronidase, chondroitinases and keratanase, for their sulphated glycosaminoglycan distributions. Glycosaminoglycan patterns were very different in the three species. Mouse lacked chemically detectable keratan sulphate, which was present in considerable amounts in rat and rabbit stroma. Mouse corneal stroma proteoglycan filaments were located predominantly at the gap zone of the collagen fibrils, mainly at the d band, with few at the a and c bands. Rat and rabbit micrographs were more complicated, with many proteoglycan filaments at the a and c, as well as the d and e bands. These findings support the proposal that the a and c bands were specific binding sites for keratan sulphate proteoglycan (Scott & Haigh, 1985b). Evidence from studies on cornea and cartilage suggests that keratan sulphate, rather than chondroitin sulphate is produced in conditions of O2 lack. Metabolic mechanisms which could account for this balance are proposed The production of uridine diphosphate glucuronic acid is the key step, which is sensitive to hypoxia, lactate and NAD:NADH ratios.
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PMID:Keratan sulphate and the ultrastructure of cornea and cartilage: a 'stand-in' for chondroitin sulphate in conditions of oxygen lack? 297 65

Chondrocytes were isolated from costal cartilage in young rats after digestion with collagenase and hyaluronidase. The immediate survival of the cells was investigated with the use of different criteria for viability, namely structural integrity and metabolic activity. Structural integrity was studied by transmission and scanning electron microscopy, trypan blue exclusion and NADH oxidation. Metabolic activity was measured both as O2 consumption and as proline and sulphate incorporation, as indicators of collagen and proteoglycan synthesis. The cellular content of glutathione was also measured. The chondrocytes isolated were found to be structurally intact and metabolically active. Early after isolation the chondrocytes varied considerably in size similarly to the native tissue. A selective loss of the larger sized cells was observed during further incubation for 24 h.
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PMID:Structural and functional integrity of chondrocytes immediately following isolation. 671 44

The influence of hyaluronidase (H) on subacute experimental myocardial ischemia was studied in isolated perfused rabbit hearts. Changes in ischemic area were assessed by epicardial nicotinamide adenine dinucleotide (NADH) fluorescence photography, an intrinsic high-resolution display of myocardial ischemia. Computerized determination of ischemic area was made from standardized photographs. Hyaluronidase was begun 20 minutes after coronary artery occlusion at 4 units/ml perfusate. NADH fluorophotographs were taken at 10-minute intervals up to 60 minutes of ischemia. Coronary sinus oxygen tension (PcsO2), myocardial oxygen consumption (MVO2), and coronary flow were determined. After 70 minutes, the hearts were perfused with rhodamine solution to identify areas of myocardial perfusion. In 13 H-treated hearts 54.3% +/- 3.7% (mean +/- SEM) of the nonperfused area (rhodamine stained) was ischemic (NADH fluorescent). In 14 untreated hearts 79.8% +/- 3.2% of the nonperfused area was ischemic (p less than 0.0001) and the ischemic areas were uniform. The distance between perfused and ischemic tissue was 952 +/- 78 micrometers in the H hearts and 504 +/- 35 micrometers in the untreated heart (p less than 0.0001). In the H hearts PcsO2 increased to 155% of the post-ligation control while it decreased to 79% in the untreated hearts (p less than 0.0001). MVO2 decreased in the H-treated hearts to 62%; the untreated hearts had no further change. In the H-treated hearts, coronary flow increased to 146% of the post-ligation control while it fell to 91% in the untreated group (p less than 0.0001). We conclude that H increases coronary flow while decreasing MVO2 during subacute ischemia. In H-treated hearts, significant amounts of myocardium remain normoxic within the nonperfused areas, and may potentially be salvaged after prolonged myocardial ischemia.
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PMID:Mechanism of action of hyaluronidase in decreasing myocardial ischemia post coronary occlusion in the isolated perfused rabbit heart. 711 92

The homolactic and catalase-deficient pathogen Streptococcus pneumoniae is not only tolerant to oxygen but requires the activity of its NADH oxidase, Nox, to develop optimal virulence and competence for genetic transformation. In this work, we show that the global regulator RegR is also involved in these traits. Genetic dissection revealed that RegR regulates competence and the expression of virulence factors, including hyaluronidase. In bacteria grown in vitro, RegR represses hyaluronidase. At neutral pH, it increases adherence to A549 epithelial cells, and at alkaline pH, it acts upstream of the CiaRH two-component signaling system to activate competence. These phenotypes are not associated with changes in antibiotic resistance, central metabolism, and carbohydrate utilization. Although the RegR(0) (where 0 indicates the loss of the protein) mutation is sufficient to attenuate experimental virulence of strain 23477 in mice, the introduction of an additional hyl(0) (where 0 indicates the loss of function) mutation in the RegR(0) strain 23302 dramatically reduces its virulence. This indicates that residual virulence of the RegR(0) Hyl(+) derivative is due to hyaluronidase and supports the dual role of RegR in virulence. This LacI/GalR regulator, not essential for in vitro growth in rich media, is indeed involved in the adaptive response of the pneumococcus via its control of competence, adherence, and virulence.
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PMID:RegR, a global LacI/GalR family regulator, modulates virulence and competence in Streptococcus pneumoniae. 1270 36