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)

Mycobacterium ulcerans produces an exotoxin in culture which, when inoculated into guinea pig skin, causes inflammation, necrosis, edema, and other histopathological changes resembling those in infections of humans. The toxin was resistant to heat and to alkalies and was moderately acid labile. Toxic activity was destroyed by Pronase, phospholipase, lipase, amylase, and glucosidase but not by trypsin, collagenase, cellulase, lysozyme, hyaluronidase, or neuraminidase. Toxic activity was resistant to treatment with 2-mercaptoethanol, urea, guanidine hydrochloride, p-chloromercuribenzoate, ethylenediaminetetraacetate, and sodium deoxycholate but was destroyed by sodium m-periodate and sodium dodecyl sulfate. The toxin was precipitated by a wide range of ammonium sulfate concentrations. Extraction with chlorofrom-methanol or petroleum ether destroyed its activity. Isopycnic density gradient ultracentrifugation in KBr produced a high-density lipoprotein layer with a 24-fold increase in specific activity. The results indicate that this toxin is a high-molecular-weight phospholipoprotein-polysaccharide complex.
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PMID:Further characterization of Mycobacterium ulcerans toxin. 3 Jun 94

The ascites form of a chemically induced guinea pig hepatoma, line-10, was resistant to killing in vitro by xenogeneic antibody and guinea pig complement. Pretreatment of line-10 cells with certain proteolytic enzymes rendered tham susceptible to the killing action of antibody and guinea pig complement. The effects of enzyme pretreatment were dependent on enzyme concentration, temperature, and could be blocked by addition of competitive or non-competitive inhibitors. The effect of the enzyme treatment could reversed by incubating the treated cells at 37 degrees C (but not at 0 degrees C), in the absence of the enzyme. Effective enzymes included ficin, bromelain, pronase, elastase, papain, trypsin, collagenase, lipases type I and type VI, and the neuraminidase preparation isolated from Clostridium perfringens. The activity of the lipase preparations and the neuraminidase preparation isolated from Clostridium perfringens appeared to be caused by proteolytic enzyme contamination. Enzyme preparations that proved ineffecitve in rendering the line-10 cells sensitive to killing by antibody and guinea pig complement included DNase, RNase, beta-glucuronidase type 6A or type B10, hyaluronidase type V or type VI, and pectinesterase.
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PMID:Lysis of tumor cells by antibody and complement. VI. Enhanced killing of enzyme-pretreated tumor cells. 17 70

The procedure of Berry and Friend for isolation of intact hepatocytes has been adapted to mouse livers. The ultrastructure of these cells was satisfactorily preserved. Isolated mouse hepatocytes secreted proteins and triacylglycerols. These secretory processes were inhibited by colchicine, indicating a likely involvement of the microtubular system for their normal occurrence. Ultracentrifugation of medium incubated with hepatocytes, followed by electrophoresis and electron microscopic examination of the floating fraction (density less than 1.006) allowed to conclude that secreted triacylglycerols were very low density lipoproteins. Glycogenolysis and lipogenesis were stimulated or inhibited, respectively, by low concentrations of glucagon (10(-10) M). Other metabolic parameters were influenced by the hormone but were less sensitive to its action. Inhibition of lipogenesis by glucagon was associated with a decrease in acetyl CoA carboxylase activity. This decrease does not appear to be related to intracellular fatty acyl-CoA accumulation secondary to hepatic lipase activation by the hormone. Insulin was effective alone or counteracted glucagon effects on lipogenesis or glycogenolysis only when exposure of cells to collagenase was held minimal. This suggests that, during isolation of hepatocytes, insulin receptors may, for unknown reasons, be more fragile than those of glucagon.
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PMID:Secretory processes, carbohydrate and lipid metabolism in isolated mouse hepatocytes. Aspects of regulation by glucagon and insulin. 17 77

Incorporation of 125I-labeled cholesterol ester rich lipoproteins from cholesterol fed rabbits into normal rabbit aorta in vitro was inhibited by heparin, lecithin, and collagenase and by succinylation of the lipoprotein. Aortic uptake of lipoprotein was increased by neuraminidase, proteases, lipase, and beta-glucuronidase. These results suggest that it may be possible to control atherogenesis by controlling the interaction of atherogenic lipoproteins with their arterial receptor.
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PMID:Control of the interaction of cholesterol ester-rich lipoproteins with arterial receptors. 18 30

To identify cells developing into adipocytes by accumulation of triglyceride, rat epididymal fat pad cells from small rats were exposed to (3)H-labeled chylomicron fatty acids in vivo and then liberated with collagenase. Tissue remnants were removed by filtration and mature fat cells by flotation. Aggregating cells were then removed by filtration through a 25- micro m nylon screen. Further purification of cells labeled in vivo was obtained by removing floating cells from those adhering to the bottom of a culture dish. The adhering cells multiplied to a confluent monolayer when cultured in Medium 199 containing serum, glucose, insulin, and a triglyceride emulsion. The cells then gradually enlarged due to granulation of the cytoplasm by a lipid-staining material. After about 2 weeks these granules had coalesced forming mature adipocytes of typical signet-ring appearance. Free adipocytes could then be recovered from the cultures by collagenase treatment. After about 2 weeks of culture these cells had the same size (about 30 micro m) as adipocytes recovered in the original collagenase preparation of the rat epididymal fat pad. They contained triglyceride lipase activity and incorporated glucose into triglycerides to the same extent as cells developed in vivo but had higher lipoprotein lipase activity. In vitro, heparin in a low concentration, prostaglandin E(1), isobutylmethylxanthine, and cholera toxin markedly promoted the development of these cells into adipocytes. This could be shown to occur almost completely indicating that this fraction of cells was homogeneous and consisted of cells with the capacity to form adipocytes. The duplication time was about 2 days and did not change with subculturing. Preadipocytes could be obtained by density gradient centrifugation, isolating triglyceride-containing cells either directly from the pad or after 3 days in culture. All of these cells developed into adipocytes as described above but did not multiply as readily. It was concluded that cells from the epididymal fat pad from small rats can be isolated in a homogenous fraction that develops in culture into cells of identical morphology and function as adipocytes formed in vivo. The differentiation of these cells into adipocytes may be manipulated in vitro.
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PMID:Isolation and characterization of cells from rat adipose tissue developing into adipocytes. 20 38

Lipolytic activity at pH 8.5-9.5 was lowered by approx. 80% in homogenates from livers perfused with collagenase or heparin. No heparin-releasable lipase activity was detected in hepatocytes isolated by collagenase treatment. It is concluded that crude collagenase completely inactivates the plasma-membrane-bound heparin-releasable lipase.
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PMID:Complete loss of heparin-releasable triacylglycerol lipase activity after collagenase treatment of the rat liver. 20 65

Collagenase is currently used in the isolation of rat hepatocytes, but it rapidly inactivates the heparin-releasable triacylglycerol lipase of the liver. Since collagenase-isolated liver cells contain a heparin-releasable monoacylglycerol hydrolase, a study was made on the effect of collagenase treatment on the substrate specificity of purified heparin-releasable lipase of rat liver. Incubation of the purified lipase with collagenase selectively decreased the triacylglycerol lipase activity of the enzyme with no effect on the monoacylglycerol hydrolase activity. Gel filtration of the lipase before and after collagenase treatment indicated cleavage of a small molecular weight fragment from the enzyme. This resulted in a preparation with less triacylglycerol lipase activity but still capable of monoacylglycerol hydrolysis.
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PMID:Modification of the substrate specificity of rat hepatic lipase by collagenase treatment. 22 27

Preincubation of normal rat soleus muscles in vitro with homogenates prepared from mixed leg muscles which had been denervated 4 days previously resulted in an increase in the contracture response to acetylcholine. After 30 min incubation a 1.5-fold increase was observed. Homogenates of normally innervated muscles did not increase the response. The active principles of the denervated muscles were found to reside in the "cytosol" fraction. An approximately 2-fold increase was observed upon incubation with the cytosol for 30 min; incubation for longer periods resulted in a subsequent decrease in the response. The effect of the denervated muscle cytosol was concentration-dependent and heat-labile. Normal muscle cytosol also increased the soleus muscle response to acetylcholine but this fraction was less effective than denervated muscle cytosol. The response of control muscles incubated in Krebs-Henseleit solution was found to decrease with time. Commercially obtained phospholipases C and D increased the response of normal soleus muscles approximatley 2-fold. Phospholipase A, lipase, trypsin, collagenase and a bacterial protease had no effect, lysozyme produced a small but consistent increase in the response to acetylcholine.
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PMID:The effect of muscle extracts on the contracture response of skeletal muscle to acetylcholine. 94 50

We have recently reported that lipase may play a role in the pathogenesis of acute pancreatitis by its ability to release fatty acids from triglycerides. The aim of this study was to further investigate the effect of lipase and its various digestive products on the integrity of isolated pancreatic rat acini. Pancreatic acini were prepared by collagenase digestion and their newly synthesized proteins labeled with 35S-methionine. Acini were later incubated in buffer to which various factors were added: Products of lipolytic digestion, such as various fatty acids and monoglycerides, fat tissue, nonactivated or trypsin activated homogenized pancreatic tissue, and a specific lipase inhibitor (THL, tetrahydrolipstatin). Cellular destruction was quantified by the degree of radiolabeled proteins released. Short chain fatty acids and monoglycerides (up to C-12) caused cellular destruction, whereas long chain fatty acids and their respective monoglycerides were not harmful. With regard to unsaturated fatty acids, long chain fatty acids (C-18 to C-22) were also able to destroy cells. The degree of cellular necrosis correlated with incubation time and fatty acid concentration. The cellular damage caused by incubation of acini with either inactive or trypsin activated pancreatic homogenates together with triglycerides could be completely inhibited by the specific lipase inhibitor THL. Bile alone caused no damage. When bile was combined with activated-pancreatic homogenates, about 25% of newly synthesized proteins were released by acini within 30 min. Incubation with a combination out of bile activated pancreatic homogenates and triglycerides resulted in the most pronounced damage. This acinar destruction could only be partly inhibited by THL. These studies suggest that both lipase and phospholipase-A2 may play an important role in the pathogenesis of acinar cell destruction.
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PMID:Isolated rat pancreatic acini as a model to study the potential role of lipase in the pathogenesis of acinar cell destruction. 128 21

Entomophthoromycosis due to Conidiobolus coronatus is a granulomatous infection characterized by lesions that originate in the inferior turbinate, spread through ostia and foramina to involve the facial and subcutaneous tissues and paranasal sinuses. The majority of the cases have been described from areas of tropical rainforest in West Africa, agricultural and outdoor workers (aged 20-60 years) being the ones most frequently affected. The fungus is common in soil and decaying vegetation. Infection probably occurs by implantation of the spores of the fungus in nasal mucosa. C. incongruus is a rare agent of the disease, so far known only from two cases with lesions involving the pericardium, mediastinum, lungs, liver, oesophagus and jejunum. C. coronatus is known to cause a clinically similar disease in horses, mules, a dolphin and a chimpanzee. A characteristic histological feature is the presence of thin-walled, broad, often septate hyphae or hyphal fragments with a thick eosinophilic sheath, frequently phagocytosed within giant cells. The fungus is known to produce in vitro several enzymes, e.g., elastase, esterase, collagenase and lipase, which have a possible role in pathogenicity. A concentrated brain heart infusion culture filtrate antigen is useful for immunodiagnosis. Several drugs e.g., potassium iodide, cotrimoxazole, amphotericin B, ketoconazole and itraconazole have been tried with varying success. Investigations on the immunology of disease and the role of proteases and lipases in the pathogenesis of infection is an important area of further research.
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PMID:Entomophthoromycosis due to Conidiobolus. 139 3


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