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

---

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

Relaxin release from dispersed luteal cells was detected by a reverse hemolytic plaque assay to determine the influence of gestational age on basal relaxin secretion. Monodispersed luteal cells were derived by collagenase treatment of corpora lutea obtained from pigs in early (days 19-26), mid-(days 47-62), and late (days 80-99) gestation. The rate of plaque development under nonstimulated conditions progressively accelerated as gestation advanced, as did the rate of increase in plaque size. These results unequivocally demonstrate that basal relaxin release increases with advancing gestation. However, only about 50% of large luteal cells released relaxin at all stages of pregnancy examined up to day 100. These data indicated not only that basal relaxin release increases during pregnancy, but also that considerable heterogeneity exists with respect to relaxin output by individual cells. In contrast, both the basal rate of relaxin release and the percentage of cells committed to relaxin release declined significantly when luteal cells derived from preparturient sows (days 107-112 of gestation) were examined. Exposure of cultured luteal cells to prostaglandin F2 alpha (10(-8) and 10(-6) M) resulted in a rapid stimulation of relaxin secretion, but this agent did not recruit additional cells into the secretory pool. These data are consistent with the idea that autonomous changes and the action of secretagogues may combine at different times to achieve overall regulation of relaxin release by the corpus luteum. The significance of nonrelaxin-releasing luteal cells remains to be determined.
...
PMID:Analysis of relaxin release from cultured porcine luteal cells by reverse hemolytic plaque assay: influence of gestational age and prostaglandin F2 alpha. 355 31

Recent evidence implicates Actinobacillus actinomycetemcomitans in the etiology of localized juvenile periodontitis. This paper reviews the morphological, biochemical and serological charcteristics of A. actinomycetemcomitans, evidence incriminating it as a periodontopathogen, its importance in human nonoral infections, and virulence factors which may be involved in the pathogenesis of A. actinomycetemcomitans infections. A. actinomycetemcomitans is a non-motile, gram-negative, capnophilic, fermentative coccobacillus which closely resembles several Haemophilus species but which does not require X or V growth factors. The organism has been categorized into 10 biotypes based on the variable fermentation of dextrin, maltose, mannitol, and xylose and into 3 serotypes on the basis of heat stable, cell surface antigens. A. actinomycetemcomitans' primary human ecologic niche is the oral cavity. It is found in dental plaque, in periodontal pockets, and buccal mucosa in up to 36% of the normal population. The organism can apparently seed from these sites to cause severe infections throughout the human body such as brain abscesses and endocarditis. There is a large body of evidence which implicates A. actinomycetemcomitans as an important micro-organism in the etiology of localized juvenile periodontitis including: (1) an increased prevalence of the organism in almost all localized juvenile periodontitis patients and their families compared to other patient groups; (2) the observation that localized juvenile periodontitis patients exhibit elevated antibody levels to A. actinomycetemcomitans in serum, saliva and gingival crevicular fluid; (3) the finding that localized juvenile periodontitis can be successfully treated by eliminating A. actinomycetemcomitans from periodontal pockets; (4) histopathologic investigations showing that A. actinomycetemcomitans invades the gingival connective tissue in localized juvenile periodontitis lesions; (5) the demonstration of several pathogenic products from A. actinomycetemcomitans including factors which may: (a) facilitate its adherence to mucosal surfaces such as capsular polysaccharides; (b) inhibit host defense mechanisms including leukotoxin, a polymorphonuclear leukocyte chemotaxis inhibiting factor, and a lymphocyte suppressing factor (c) cause tissue destruction such as lipopolysaccharide endotoxin, a bone resorption-inducing toxin, acid and alkaline phosphatases, collagenase, a fibroblast inhibiting factor and an epitheliotoxin.(ABSTRACT TRUNCATED AT 400 WORDS)
...
PMID:Actinobacillus actinomycetemcomitans in human periodontal disease. 388 66

With an increasing interest in the role of the monocyte-macrophage in the pathogenesis of atherosclerosis and as a progenitor of plaque intimal foam cells, a model for the study of foam-cell differentiation in an extravascular environment has been developed. Granulomas were induced in 25 normocholesterolemic (NC) and 28 hypercholesterolemic (HC) rabbits by the subcutaneous injection of 15 ml of 1% carrageenan. Granuloma tissue was harvested at 4, 7, 14, and 28 days and studied by light and transmission electron microscopy. Macrophages and foam cells were isolated by enzymic dispersion with collagenase and cultured for further characterization by scanning electron microscopy, nonspecific esterase (NSE), and oil red O (ORO) staining. Granuloma macrophages from NC rabbits were consistently ORO-negative, contrasting with those from HC rabbits which were strongly ORO-positive, even at 4 and 7 days. With an increasing duration of exposure to hypercholesterolemia, macrophages accumulated increasing amounts of stainable lipid, and in the 28-day HC granulomas, large foam cells distended by lipid inclusions accounted for 70% of the cells present. This model has established that NSE-positive macrophages in HC granulomas accumulate lipid and assume the morphologic characteristics of atheromatous intimal foam cells.
...
PMID:Evolution of foam cells in subcutaneous rabbit carrageenan granulomas: I. Light-microscopic and ultrastructural study. 396 33

Hepatocytes were isolated from 1-day and 1,2,3 and 12-week old rat livers by collagenase perfusion and the relative numbers of albumin (ALB) and alpha-fetoprotein (AFP) producers were evaluated using the reverse hemolytic plaque assay. The percentage of ALB producers remained essentially constant to 35% over the 12-week period. In contrast, the percentage of AFP producers varied from 19% at 1 day up to 28% at 1 week and then down to 0.1% at 3 weeks. Moreover, a double identification of secreting hepatocytes, using an adaptation of the plaque assay, demonstrated that AFP producing hepatocytes were also ALB producers. These results are explained in terms of a restricted specialization of differentiating hepatocytes during normal development.
...
PMID:Restricted specialization of differentiating hepatocytes in terms of albumin and alpha-fetoprotein production. 616 64

Oral administration of 2-mercapto-2-methylpropanoyl-L-cysteine (SA 96), a newly synthesized sulfhydryl compound, showed protective and curative effects on adjuvant-induced arthritis in rats similarly to those seen with D-penicillamine (D-PA). However, the effects of these compounds were not dose-dependent, and the maximum effects of SA96 were observed at 10 mg/kg/day. On the contrary, SA96 and D-PA had little effect on the various acute and subacute inflammatory responses induced in rat and mice. Formation of hemolytic plaque forming cells in the spleen of mice immunized with 5 X 10(8) sheep red blood cells was potentiated by the oral administration of both compounds. These stimulatory effects of SA96 and D-PA on the humoral immune responses were also not dose-dependent, and the maximum effects of SA96 were observed with 10 mg/kg/day, as in the case of adjuvant-induced arthritis in rats. In in vitro experiments, the inactivation of rheumatoid factor and the inhibition of collagenase and bone alkaline phosphatase activities were observed with both compounds, but these effects of SA96 were more potent than those of D-PA. As there is a similarity in the pharmacological profiles of SA96 and D-PA, SA96 may prove to be clinically effective for rheumatoid arthritis.
...
PMID:[Pharmacological studies of new sulfhydryl compounds 2-mercapto-2-methylpropanoyl-L-cysteine (SA96). I. Evaluation of anti-rheumatic action (author's transl)]. 624 2

Medroxyprogesterone, dexamethasone, or cortisone, locally applied in sustained release polymer to rabbit V2 carcinoma implanted in the rabbit cornea, blocked neovascularization and three-dimensional growth of the tumor. These hormones similarly prevented the vascular proliferative response to implants in the rabbit cornea of mouse B-16 melanoma and also the response to implants of polymer containing tumor extract with angiogenesis activity. The inhibitory responses were accompanied by considerable reduction in collagenolytic activity released into culture medium by explants of the two tumors and of the corneal region containing angiogenic hepatoma extract. Morphologic studies revealed extensive three-dimensional disruption of the compact laminated collagenous structure of the cornea by untreated V2 carcinoma. In the presence of hormone the tumor grew slowly as a noninvasive two-dimensional plaque limited to the narrow region of the insertion pocket in the cornea, with no obvious disturbance of structure elsewhere. Cortisone was much les effective than medroxyprogesterone or dexamethasone. Testosterone and estradiol had no effect on the three measured properties. The data suggest that local hormonal interference with neovascularization, collagenase production, and tumor growth can prevent neoplastic invasion and destruction of a dense collagenous connective tissue.
...
PMID:Inhibition of tumor growth, vascularization, and collagenolysis in the rabbit cornea by medroxyprogesterone. 626 56

This pilot study was designed to test the feasibility of using purified clostridial collagenase in the clinical management of Peyronie's disease. The basic properties of this agent are discussed. We studied its effect on Peyronie's plaque tissue by a quantitative in vitro assay utilising the liberation of free alpha-amino groups as an index of enzymatic collagenolysis. Tissue from three patients with Peyronie's disease was used. Tunica albuginea from a second group of three normal patients was studied in the same manner, and no selectivity for the collagen of Peyronie's plaques was identified. Utilising human pericardium as a uniform collagenous substrate, a simple dose-effect relationship was established, and the distribution characteristics of injected collagenase observed. Its effects on blood vessels and nerves in vivo was determined as well as the effects of collagenase on the histology of normal and diseased human tissue in vitro. A tentative dose for use in Peyronie's disease was established, which is discussed in light of existing toxicological data. The study was designed to test the feasibility of purified collagenase in the clinical management of Peyronie's disease. Data included detail plaque digestion and dose-effect relationships in vitro, as well as the histological effects on plaques, blood vessels, and nerves in vivo and in vitro. It is concluded that collagenase may warrant further clinical testing in the treatment of Peyronie's disease.
...
PMID:Collagenase for Peyronie's disease experimental studies. 629 Dec 16

Basement membranes in human gingiva are found in dento-epithelial junction, epithelial-connective tissue junction and endothelium-connective-tissue junction where they have important attachment and filtering functions. The ability of plaque and gingiva-derived proteinases to degrade Type IV collagen, the major protein of basement membranes, was examined in vitro. The basement membrane collagen (Type IV) isolated from bovine lens capsules was incubated in the presence of enzyme samples. The degradation was assayed by the release of hydroxyproline from the insoluble substrate and by examining the peptide pattern of the residue by polyacrylamide gel electrophoresis. Salt extracts of inflamed gingival specimens degraded basement membrane collagen into soluble form and produced degradation products that were similar to those produced by human leukocyte extracts. Gingival crevicular fluid collected from patients with severe adult periodontitis also digested the substrate but the degradation pattern was different from the leukocyte and gingival extract samples. The pattern closely resembled the degradation produced by bacterial plaque extracts. A third type of cleavage was observed when collagenase from Clostridium histolyticum was incubated with basement membrane collagen. Crevicular fluid and the extracts from gingiva, leukocytes and plaque also contained gelatinase and elastase-like enzyme activities that have earlier been shown to be potent in degrading basement membrane. It was concluded that enzymes capable of degrading basement membrane collagen in gingivitis and periodontal disease may originate from both plaque bacteria and human leukocytes. It also appeared that the enzymes responsible are more likely to be gelatinase and elastase-like enzymes than specific collagenases.
...
PMID:Degradation of basement membrane collagen by proteinases from human gingiva, leukocytes and bacterial plaque. 631 10

Surface markers of human gingival fibroblasts in vitro were investigated using monoclonal and heterologous antisera against a range of cell surface antigens, together with rosetting techniques to characterize surface receptors for IgG and C3. WI-38 fibroblasts and human peripheral blood monocytes were used as control cells. Human gingival fibroblasts exhibited complement receptors and beta2-microglobulin, as did WI-38 cells. Ten per cent of the human gingival fibroblasts were positive for HLA-DR antigens and additionally exhibited a granulocyte antigen not apparent on WI-38 cells. Monolayers of the gingival fibroblasts were further exposed for short periods to varying concentrations of enzymes (trypsin, collagenase and neuraminidase), bacterial extracts (lipopolysaccharide and lipoteichoic acid) and crude supra- and subgingival plaque sonicates. Surface-marker analysis was then carried out. The most noticeable effects were obtained with Vibrio cholerae neuraminidase which enhanced C3 receptor and surface antigen expression, and supragingival plaque sonicate which depressed the expression of HLA-DR and granulocyte antigens while not affecting beta2-microglobulin expression. Trypsin reduced antigen expression to a degree, but its effects were mainly on cell adherence.
...
PMID:Surface markers of human gingival fibroblasts in vitro. Characterization and modulation by enzymes and bacterial products. 633 Mar 32

The Tyzzer's disease organism was grown in primary monolayer cultures of adult mouse hepatocytes prepared by collagenase perfusion. The organisms produced a plaque-like cytopathic effect involving almost the whole culture around 72 h post-infection when the bacterial growth reached a maximum. The organisms showed specific immunofluorescence, and electron microscopy revealed that intracellular organisms had peritrichous flagella and underwent cell division. After intravenous inoculation of the infected cell culture into mice, necrotic hepatitis was produced and the organisms, recovered from the liver lesion, could be propagated in primary culture of mouse hepatocytes.
...
PMID:Growth of Tyzzer's organism in primary monolayer cultures of adult mouse hepatocytes. 634 4


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>

---