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)

Adult CBA/HZgb mice islets harvested by collagenase digestion were injected intraperitoneally in 52 singeneic diabetic recipients (CBA/Hgb leads to CBA/HZgb, 450-600 islets per mouse). Normal serum glucose levels, 24-h urine volume, insulin levels and body weight were completely restored to normal in all recipients during the next 2-5 months. Immunological function was assessed in control, diabetic and diabetic-transplanted mice by following their responses to sheep erythrocytes (expressed as the number plaque-forming cells in the spleen). In transplanted mice, the plaque-forming cell responses were as follows: 1 month after transplantation--43% of the plaque-forming cell counts in control (normal, non-diabetic) mice; 2 months after transplantation--56% of the control value; and 94% of the control value after 5 months. Ten months after the transplantation, the plaque-forming cell counts were slightly above the control value (148%). It appears, therefore that transplantated islet tissue positively affects the immunological as well as the diabetic state of the recipients.
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PMID:Recovery of the immune system in diabetic mice after transplantation of isolated islets of Langerhans. 643 64

A technique has been developed for isolating cells from the intimal and medial layers of the human aorta by enzymatic dispersion. After mechanical separation of intima, media and adventitia the intima and the media were dispersed by collagenase and elastase. Enzyme-isolated cells seeded in the culture with at a frequency of 30 to 50%. In the primary culture differentiated aortic cells were morphologically heterogenous. It was possible to define four main types of cells according to their shape: polygonal, elongated, asymmetrical and stellate. Polygonal and stellate cells are found only in cultures of grossly normal intima, whereas elongated and asymmetric cells are found in practically all cultures. The ratio of elongated to asymmetric cells in cultures obtained from healthy aorta and atherosclerotic plaque is more or less the same at approximately 3:1. In cultures of fatty streaks the proportion of asymmetric cells exceeds 50%. Using immunofluorescence, all four types of cell were identified as smooth muscle cells. The possible reasons for the cellular polymorphism in primary culture and the prospects of utilizing this culture for the study of cellular aspects of atherosclerosis' pathogenesis are discussed.
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PMID:Primary cultures of enzyme-isolated cells from normal and atherosclerotic human aorta. 651 17

Mononuclear cells were isolated from the mucosa and submucosa of small intestine and colon of 22 subjects with localized, anatomically remote disease and four subjects with Crohn's disease (nine specimens) by sequential treatment with EDTA and collagenase. The effects of isolation techniques on cell yields and viability were examined. Secretion of specific IgA, IgM and IgG antibodies to common faecal Escherichia coli strains by individual mononuclear cells was studied using a haemolytic plaque assay. A majority of specific antibody secreting cells secreted IgA antibody. This response was greatest and most consistent in the distal colon but extended from stomach to rectum. There was no evidence of a primary defect in IgA antibody response in the few subjects with Crohn's disease available for study.
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PMID:Escherichia coli antibody-secreting cells in the human intestine. 680 77

The role of crowded teeth in the etiology of attachment loss was studied in thirty teeth extracted for orthodontic reasons from eight children 12 to 13 years of age. Following extraction, the teeth were stained in a 1 percent solution of water blue and examined under the stereomicroscope. In one third of the thirty teeth, a 0.9, 2.0, and 3.5 mm. loss of attachment was observed on surfaces adjacent to which another tooth had erupted into an extremely crowded environment. On the same surfaces, subgingival plaque had grown down to the area of the cementoenamel junction. The premature loss of attachment was assumed to be mediated by collagenase derived from the regressing dental organ or from the junctional epithelium surrounding the erupting teeth. The premature downgrowth of subgingival plaque to the area of the cementoenamel junction was facilitated by the development of an irregular contact line within the interdental papilla, rather than a contact point above the papilla.
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PMID:Eruption of teeth into crowded position, loss of attachment, and downgrowth of subgingival plaque. 693 53

Attempts were made to isolate adherent phagocytic cells (macrophages) from mouse Peyer's patch cell suspensions. Cell suspensions prepared by teasing apart the Peyer's patches contained no adherent phagocytic cells. However, if Peyer's patch fragments were treated with collagenase to disrupt the tissue matrix, cells prepared in this way contained a subpopulation of adherent phagocytic cells. These cells comprised only 0.1-0.2% of the total nucleated cell population of the Peyer's patch. Similar cells could also be isolated from the Peyer's patches of germ-free mice, but as judged by their ability to ingest opsonized erythrocytes, these cells were less activated than cells from the Peyer's patches of normal mice. Adherent cells from the Peyer's patches of normal mice could present antigen (ovalbumin) to T cells, and Peyer's patches cell suspensions containing adherent cells could be stimulated in vitro to produce an anti-sheep red blood cell plaque-forming cell response in the absence of 2-mercaptoethanol. These studies show that although the frequency of phagocytic adherent cells is extremely low in Peyer's patches, these cells have functions consistent with that of adherent cells in other lymphoid tissues.
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PMID:Isolation and functional characteristics of adherent phagocytic cells from mouse Peyer's patches. 706 73

Human polymorphonuclear leukocytes (PMN) chemotaxis was tested during exposure to leukocyte and platelet extracts, a variety of polyelectrolytes, inflammatory exudates, and bacterial products. The chemoattractants employed were either zymosan-activated serum or supernatant from autolyzed Staphylococcus aureus. Chemotaxis to both chemoattractants was markedly inhibited by leukocyte and platelet extracts; inflammatory exudates; anionic polyelectrolytes, DNA, hyaluronic acid, liquoid; and by cationic polyelectrolytes, histone, protamine base, protamine sulfate, and myeloperoxidase. Inhibition was also found with elastase, collagenase, pepstatin, and epsilon-amino-caproic acid. Bacterial products, such as lipoteichoic acid and lipopolysaccharides, and extracts of human dental plaque inhibited chemotaxis. No inhibition of chemotaxis was observed with heparin (< 10 micrograms/ml), chondroitin sulfate, phosphatidylethanolamine and phospatidylserine. Indeed, chondroitin sulfate markedly enhanced chemotaxis and antagonized the inhibitory effect of leukocyte or platelet extract. None of the agents employed was toxic to PMN as judged by trypan blue exclusion. These observations suggest that cationic polyelectrolytes and inflammatory exudates influence PMN surfaces, modifying interaction with chemoattractants. Assessment of the role of PMN chemotaxis in host defense against microbial invaders requires evaluation of the response in the presence of agents likely to be present in inflamed tissues.
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PMID:Modulation of human polymorphonuclear leukocyte chemotaxis by leukocyte extracts, bacterial products, inflammatory exudates, and polyelectrolytes. 742 9

Degradation of the atherosclerotic plaque extracellular matrix could destabilize the lesion, rendering it more prone to rupture. Both macrophages and vascular smooth muscle cells (SMCs) are potential sources of matrix metalloproteinases (MMPs), secreted enzymes that can digest vascular matrix. We explored interactions between human vascular SMCs and human monocytes that result in the secretion of interstitial collagenase (MMP-1) and stromelysin (MMP-3). Monocytes alone or those treated with SMC-conditioned media did not secrete these metalloproteinases as detectable by Western blot analysis. SMCs increased secretion of both MMP-1 and MMP-3 greater than 20-fold when cocultured with monocytes or when treated with monocyte-conditioned media. Addition of macrophage colony stimulating factor (< or = 1000 U/mL) to cocultures of monocytes and SMCs did not affect metalloproteinase secretion. Recombinant interleukin (IL)-1 receptor antagonist inhibited MMP-1 and MMP-3 induction in SMC cultures treated with monocyte-conditioned media (94% and 96% reduction, respectively), while a neutralizing antibody to tumor necrosis factor-alpha had no significant effect on metalloproteinase secretion. In contrast to the induction by monocyte-conditioned media of MMP-1 and MMP-3 secretion by SMCs, monocyte-conditioned media did not increase secretion of 72-kD gelatinase (MMP-2). Thus, monocytes induce MMP-1 and MMP-3 secretion by vascular SMCs through an IL-1-dependent mechanism. This response of SMCs to a defined macrophage product may contribute to plaque destabilization by mononuclear phagocytes in the lesion.
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PMID:Human vascular smooth muscle cell-monocyte interactions and metalloproteinase secretion in culture. 748 54

The reverse hemolytic plaque assay (RHPA) uses complement-mediated red blood cell lysis to detect peptide secretion by individual cells. Initially, the RHPA was used to study the function of neurons and B lymphocytes. More recently, the RHPA has been adapted to measure hormone release from individual pituitary, parathyroid, luteal, and pancreatic islet cells. We have applied this technique to detect insulin-like growth factor binding protein-1 (IGFBP-1) secretion by a human hepatoma cell line (HepG2). We proposed that the technique of RHPA could be used to study peptide release from single hepatocytes in various defined conditions. Our goal was the study of the kinetics of IGFBP-1 secretion from hepatoma cells and rat hepatocytes and to determine the heterogeneity of the cell population regarding the secretion of IGFBP-1. To evaluate the optimal conditions of IGFBP-1 secretion by hepatoma cells and rat hepatocytes and to evaluate the influence of cell dispersion on hepatocyte's behavior, we evaluated three techniques of cell dispersion: trypsin digestion, collagenase digestion, and mechanical dispersion. We tested cell viability, determined the percentage of secreting cells versus non-secreting cells, and measured mean plaque area which is a function of the amount of IGFBP-1 secreted by an individual cell. We determined the optimal IGFBP-1 antibody dilution for the detection of secreted IGFBP-1 by hepatocytes, evaluated the initiation of IGFBP-1 secretion from cultured cells, and quantified time-dependent IGFBP-1 secretion. In addition to demonstrating the feasibility of measuring IGFBP-1 from a cultured cell line, we measured IGFBP-1 release from freshly dispersed rat hepatocytes.
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PMID:Secretion of insulin-like growth factor binding protein-1 from individual hepatocytes. 753 Jan 14

Dental plaque is the major aetiological factor in periodontal diseases and contains several proteolytic enzymes. The origin of these proteinases is, however, poorly studied. This study was undertaken to characterize collagenase present in dental plaque of adult periodontitis patients. Vertebrate-type rather than bacterial-derived collagenase activity was detected in extracts of both supra- and subgingival dental plaque extracts of adult periodontitis patients. Dental plaque collagenase was found to exist predominantly in autoactive form. Dental plaque collagenase from periodontally healthy individuals existed in latent from. Latent dental plaque collagenase from periodontitis lesions could be activated by a 95 kD chymotrypsin-like proteinase from Treponema denticola and human leukocyte cathepsin G but not by human plasmin. Incubation of purified latent leukocyte collagenase with whole cells of Fusobacterium nucleatum, Eubacterium saburreum, Prevotella buccae and Porphyromonas gingivalis, however, did not result to the activation of the enzyme. Doxycycline in vitro inhibited dental plaque collagenase with an IC50-value of 20 microM. Dental plaque collagenase degraded more efficiently type I and II collagens than type III collagen. Western-blot analysis with specific anti-human neutrophil collagenase-antibody revealed that both in supra- and subgingival dental plaque extracts dental plaque collagenase had undergone proteolytic conversion from an 80 kD proform to a 58 kD active form which is associated with catalytic autoactivity as measured by functional collagenase assay. This reflects proteolytic activation of leukocyte collagenase in dental plaque probably by other proteases derived from potent periodontopathogenic bacteria such as T. denticola or other PMN proteases such as cathepsin G.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cellular source, activation and inhibition of dental plaque collagenase. 759 2

Periodontal diseases essentially comprise a group of oral infections whose primary aetiological factor is dental plaque. Removal of the cause (and its effects) is the primary aim of both non-surgical and surgical treatment regimens, although the infective nature of the diseases has led to the widespread use of antimicrobials as an adjunct to mechanical debridement. The tetracyclines are primarily bacteriostatic agents that are effective against many Gram-negative species including putative periodontopathogens such as Actinobacillus actinomycetemcomitans (A.a.). The proven efficacy of this group of drugs in the management of periodontal diseases may be related not only to their antibacterial actions, but to a number of additional properties that have been recently identified. These include collagenase inhibition, anti-inflammatory actions, inhibition of bone resorption and their ability to promote the attachment of fibroblasts to root surfaces. Consequently, tetracyclines have also been used as an adjunct to bone grafting in periodontal defects, and as agents for 'conditioning' root surfaces to enhance the regeneration of periodontal tissues. When tetracyclines are taken orally, consideration must be given both to the potential unwanted effects and to interactions with other drugs that are taken concurrently. Such problems are minimised however, when the drugs are incorporated into controlled, slow-release formulations which are currently being researched and marketed for intra-oral use.
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PMID:Tetracyclines in the management of periodontal diseases. A review. 770 36


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