Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.4.24.3 (collagenase)
18,340 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Four cases of human keratitis caused by the tropical fungus Lasiodiplodia theobromae have been encountered in Miami, Florida bringing to 8 the number of cases reported in the world literature. Two of the ulcers were mild. Three patients recovered without severe impairment of vision after topical polyene treatment, but 1 patient with a severe ulcer required therapeutic keratoplasty after 11 days of topical natamycin. Histopathology revealed fungus deep in the cornea, invading Descemet's membrane. L. theobromae appeared to have collagenase activity in vitro. Inoculation of L. theobromae into the corneas of rabbits produced progressive ulcers. The fungus was endemic in Miami on home grown and imported bananas. Polyene antimycotic antibiotics were fungicidal for L. theobromae in vitro. Thiabendazole was effectively fungistatic but varied in fungicidal effect. Clotrimazole and miconazole were only incompletely fungistatic. Of 7 strains of L. theobromae tested, 4 were relatively resistant to 5-flurocytosine.
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PMID:Lasiodiplodia theobromae as a cause of keratomycoses. 108 94

The author presents a case with spontaneous perforation of the cornea after extracapsular cataract extraction in a female patient with rheumatoid arthritis. Systemic disorganization of the connective tissue and elevated collagenase activity essentially contribute to the pathogenesis of corneal perforation. Therefore, besides antibacterial drugs, collagenase inhibitors, 3% aqueous solution of cysteine, antimeasles gamma-globulin, and a regeneration stimulant, 5% ascorbic acid aqueous solution, were used in the treatment. The pathogenetic therapy was conducive to early healing of the corneal defect and helped save the eye and preserve its good function (0.8 s + 10.0 diopters).
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PMID:[Pathogenetic therapy of spontaneous corneal perforation after extracapsular cataract extraction]. 128 54

Collagen shields applied to the corneas of patients with bacterial keratitis degrade rapidly, often within a few hours. Once treatment brings the infection under control, subsequently applied collagen shields degrade more slowly. In vitro models were established to evaluate the significance of these observations. Twenty-four and 72-hour collagen shields were incubated with collagenase from Clostridium histolyticum. The in vitro rate of digestion of the shields was directly proportional to the concentration of collagenase, with the rate of digestion of the 24-hour shields being greater than that of the 72-hour shields. Therefore, the rate of collagen shield degradation may be a clinically useful index of collagenase activity on the ocular surface. Ultrastructural studies of collagen shields from patients with acute bacterial keratitis revealed irregular degradation of shield matrix with no evidence of adherence of microorganisms or inflammatory cells. Co-incubation of deepithelialized rabbit corneas and collagen shields resulted in inhibition of the digestion of the rabbit corneas when the weight:weight ratio of collagen shield:rabbit cornea was increased to greater than or equal to 2:1. Collagen shields may inhibit corneal collagen degradation in infectious ulceration and melting disorders by effectively competing for collagenase on the ocular surface.
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PMID:The collagen shield as a collagenase inhibitor and clinical indicator of collagenase activity on the ocular surface. 131 47

The expression and localization of type I collagen and collagenase gene were studied by in situ hybridization using rabbit cornea during wound healing following epikeratophakia or alkali-burn. In corneas 24 days after epikeratophakia, alpha 1(I) collagen mRNA was detected in keratocytes which had migrated from the host cornea into the keratolens. In contrast, collagenase mRNA was detected in cells which seemed to be inflammatory cells around the suture between the host stroma and the keratolens. The increase of alpha 1(I) collagen mRNA in keratocytes was observed in corneas 94 days after epikeratophakia and in alkali-burned corneas 1-2 months after the burn. These results provide evidence that keratocytes synthesize collagen and that this synthesizing activity lasts for a long period during corneal wound healing.
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PMID:Localization of collagen (I) and collagenase mRNA by in situ hybridization during corneal wound healing after epikeratophakia or alkali-burn. 132 24

We have previously recovered herpes simplex virus type 1 (HSV) from the corneas of latently infected mice by cultivation in vitro. It could be argued, however, that these data do not definitively distinguish between persistent and latent corneal infection. We have now used RNA hybridization in situ to resolve this question by determining the expression of HSV genes in the corneas of BALB/c mice during latent infection. Two to four months after topical corneal inoculation with HSV, when no active ocular disease or infectious virus was present, corneas were removed and digested with collagenase. Dissociated cells pooled from two corneas were hybridized with 3H- or 35S-labeled 2.6-kb single-stranded RNA probes to detect sense and antisense ICP-0 transcripts. Twenty-five percent of the pools hybridized with the probe for antisense ICP-0 (latency-associated transcript, LAT), while only 3% hybridized with the probe for ICP-0 (p less than 0.03). Of the cells in positive pools, 0.6-7.0% showed a positive hybridization signal for LAT. No infectious virus was found by culture of supernatants from the probed pools or control latently infected corneas. These data provide further evidence that HSV can establish a true latent infection in the mouse cornea.
Cornea 1992 Sep
PMID:Detection of herpes simplex virus type 1 latency-associated transcripts in corneal cells of inbred mice by in situ hybridization. 133 Apr 38

The aim of this study is to optimize conditions for growing endothelial cells on vascular biomaterials. Bovine cornea endothelial cells (BCEC), stimulated by basic Fibroblast Growth Factor (bFGF) secrete an extracellular matrix (ECM) similar to the Descemet membrane produced in vivo by these cells. This ECM, obtained by removing BCEC with an hypotonic shock can be used as a substratum for other endothelial cell growth. Human endothelial cells (HEC) were purified from omentum that was digested with a solution of collagenase-dispase, then filtered through nylon meshes. The cells were further purified by centrifugation onto a Percoll gradient. A comparative study on the attachment and growth of HEC on various coatings (laminin, poly-L-lysine, fibronectin or ECM) indicates that ECM is the most performing substratum. The quality of this endothelium was confirmed by the presence of factor VIII, and MHC class I and the absence of class II antigens.
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PMID:Extracellular matrix covered biomaterials for human endothelial cell growth. 149 48

Activation of the neutrophil respiratory burst by the supernatant fraction from an alkali-treated collagen preparations (SAC) was enhanced by longer durations of exposure to alkali (1 N NaOH for 0.5-24 hr). The concentrate obtained from ultrafiltration (greater than 30,000 molecular weight) of SAC (1 N NaOH for 24 hr) retained the stimulatory factor. Fractionation of this ultraconcentrate by high-performance liquid chromatography showed that the stimulatory activity resided in the void volume (highest molecular weight). The amino acid composition of this active fraction revealed that this proteinaceous stimulant was not derived from the collagen molecule. Treatment of the SAC with ultrapure bacterial collagenase increased its stimulatory capacity, confirming its noncollagenous nature. Alkali treatment of whole cornea also released a similar large molecular weight, noncollagenous protein that stimulated the respiratory burst of polymorphonuclear leukocytes. Enhanced stimulation after prolonged NaOH treatment of the collagen preparation or collagenase treatment of SAC suggests that the stimulant might reside between collagen fibrils and then be released as the matrix is degraded.
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PMID:Amino acid composition of a neutrophil respiratory burst stimulant. Evidence for a protein, noncollagenous source. 164 76

Proteolytic enzymes, particularly collagenase, are involved in development of eye cornea chronic ulcers. Analysis of lacrimal fluid obtained from the patients enabled to find not only the collagenase activity but and serine enzymes exhibiting BAEE esterase activity. Plasmin, blood plasma and tissue kallikreins regulated permeability of capillaries in conjunctiva and lacrimal gland as well as they activated latent collagenase. Studies of BAEE esterase activity in lacrimal fluid of the patients are required for prescription of adequate pathogenetic treatment.
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PMID:[Proteolytic enzymes of the lacrimal fluid as pathogenesis factors of chronic corneal ulcer]. 169 16

We previously demonstrated that there are two waves of increased collagen synthesis following corneal laceration in rabbits. In the present study, we have examined whether increases in collagen synthesis and degradation result from increased amounts of mRNAs for collagen and collagenase, respectively. Rabbits were anesthetized by combined administration of ketamine (intramuscular) and pentobarbital (intravenous). A penetrating 8-mm incision was made at the center of each cornea. The lacerated corneas were allowed to heal for 0-49 days. The rabbits were then killed and the corneas excised. The total RNA was extracted from the tissue and subjected to slot-blot hybridization using 32P-labeled alpha 1(I) cDNA. The results indicate that there is a two-phase increase in the amount of alpha 1(I) mRNA in injured corneas and that the collagenase mRNA is elevated at most times throughout the healing period. However, the increase is collagenase mRNA may not fully account for the accelerated collagen degradation during corneal wound-healing. Thus, we propose that cells in the wound area may be directly involved in collagen degradation by phagocytosis. To examine our hypothesis, we cultured injured rabbit corneas in the presence or absence of leupeptin, a proteinase inhibitor. The tissues were then examined by electron microscopy. In the presence of leupeptin, lysosomes within fibroblasts or fibroblast-like cells in the wound area of the lacerated corneas healed for 2 and 3 weeks, contain collagen fibrils. In the absence of leupeptin no identifiable collagen was seen in the lysosomes.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Collagen metabolism during healing of lacerated rabbit corneas. 184 30

We report the occurrence of sterile corneal ulceration in 11 eyes of eight patients with collagen vascular diseases and dry eyes after cataract extraction with intraocular lens implantation. Keratolysis occurred after both extracapsular and intracapsular cataract extraction and appeared unrelated to the type of intraocular lens. Despite aggressive lubrication and other medical treatment, including systemic immunosuppressive agents, penetrating keratoplasty was often required. Although all eyes were saved, visual outcome was usually poor. The histopathologic finding of polymorphonuclear leukocytes localized near the areas of corneal dissolution provides evidence for the role of polymorphonuclear leukocyte-derived collagenase as a contributing factor in the pathogenesis of sterile corneal ulceration in these patients.
Cornea 1990 Oct
PMID:Sterile corneal ulceration after cataract extraction in patients with collagen vascular disease. 207 56


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