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)

The total protein-synthesizing and collagen-synthesizing activities of poly(A)-containing RNA from the membrane-bound polyribosomes of chicken embryos were studied under various conditions in a cell-free wheat germ system. The optimal concentrations of poly(A)-RNA, mono- and bivalent cations and spermine necessary for the translation of collagen and non-collagen proteins were determined. It was shown that within a wide range of K+ and Mg2+ concentrations in a cell-free system the poly(A)-RNAs studied are very actively involved in the translation of non-collagen proteins. At the same time the bacterial collagenase-cleavable polypeptides synthesized on poly(A)-RNA from the membrane-bound polyribosomes were identified only after addition of polyamine -- spermine (40 mk/M) to the system. In this case the relative level of collagen polypeptide synthesis remains constant within a wide range of concentrations of mRNA, K+ and Mg2+ in the system. Collagen-synthesizing activity of poly(A)-RNA from membrane-bound polyribosomes in a heterologous cell-free system as compared to that of membrane-bound polyribosomes in a homologous system showed that these polyribosomes can be effectively used for isolation of collagen mRNA.
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PMID:[Biosynthesis of collagen in a cell-free system from wheat germ on poly(A)-RNA isolated from membrane-bound polyribosomes of chicken embryos]. 721 40

Biochemical and morphological properties of rat hepatic parenchymal cells isolated without calcium were compared to cells isolated by adding calcium to the isolation medium at the time of addition of collagenase. Calcium contents of the two cell preparations were 4.5 +/- 0.3 and 10.5 +/- 0.5 nmol/mg dry wt, respectively (P les than 0.001). Magnesium content of both preparations was 37 nmol/mg dry wt. Potassium contents were 92 and 154 meq/l, respectively (P less than 0.001). Potassium content of calcium-deficient cells increased to 161 meq/l following incubation for 30 min in a medium containing 1.6 mM ionized calcium. When incubated in a medium containing a subphysiologic concentration of ionized calcium, calcium-deficient cells rapidly lost the ability to exclude trypan blue and to retain lactate dehydrogenase activity. As contrasted to calcium-sufficient hepatocytes, calcium-deficient cells failed to accumulate alpha-aminoisobutyric acid by active transport and lacked microvilli and nuclear contents. This study supports simultaneous addition of calcium and collagenase to the isolation medium as a means for preserving physical, functional, and morphological integrity of isolated hepatic parenchymal cells.
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PMID:Deleterious effects of calcium deprivation on freshly isolated hepatocytes. 724 60

Magnesium transport across the plasma membrane of cardiac and liver cells appears to be under hormonal control. The increase in cytosolic cAMP, following the adrenergic stimulation of both cell types, results in a major Mg2+ efflux from perfused rat hearts or livers and from collagenase-dispersed ventricular myocytes or hepatocytes. By contrast, the activation of protein kinase C by carbachol, vasopressin, phorbol-myristate acetate or diacylglycerol analogs induces Mg2+ accumulation in either of the experimental models. As for the role of intracellular compartments on Mg2+ homeostasis, the cAMP-mediated Mg2+ efflux largely depends on the mobilization of Mg2+ from mitochondria via the mitochondrial adenine nucleotide translocase. By contrast, Mg2+ influx appears to be related to the endo(sarco)plasmic reticulum and its dynamic handling of cytosolic Ca2+.
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PMID:Cell magnesium transport and homeostasis: role of intracellular compartments. 826 15

Prostatic carcinoma cells have a propensity to metastasize to bone, and we propose that this phenomenon may be promoted by the adhesion of metastatic cells to bone matrix. Bone matrix is produced by osteoblasts, and we have developed an in vitro model of bone matrix by isolating the substratum deposited by human osteoblast-like U2OS cells. The collagenous nature of this matrix was demonstrated by the incorporation of [3H]proline and its subsequent release by purified collagenase. Both U2OS matrix and purified type I collagen stimulated the adhesion of human PC-3 prostatic carcinoma cells. Human laminin supported adhesion to a much lesser extent, and PC-3 cells did not adhere to fibronectin. Adhesion of PC-3 cells to U2OS matrix closely resembled adhesion to purified type I collagen with respect to (a) inhibition by a collagen-derived peptide and by antibodies raised against alpha 2 or beta 1 integrin collagen receptor subunits; (b) lack of inhibition by RGD (Arg-Gly-Asp) peptides; (c) stimulation by Mn2+ and Mg2+ ions but not by Ca2+ ion; and (d) stimulation by the phorbol ester PMA (phorbol 12-myristate 13-acetate). This adhesion was also stimulated (2.3-fold) by transforming growth factor beta (TGF-beta), which is a major bone-derived growth factor. We conclude that human osteoblast-like matrix is an adhesive substrate for PC-3 prostate carcinoma cells. This adhesion appears to be mediated by the interaction of alpha 2 beta 1 integrin on PC-3 cells with matrix-derived collagen. The stimulation of this adhesion by TGF-beta suggests that the co-expression of TGF-beta and type I collagen in bone may synergistically facilitate the adhesion of metastatic cells to bone matrix proteins and thereby increase their localization in the skeleton.
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PMID:Bone cell matrix promotes the adhesion of human prostatic carcinoma cells via the alpha 2 beta 1 integrin. 852 12

Magnesium ion (Mg2+) is a bronchodilator, but little is known about its mechanism of action on airways. We hypothesized that Mg2+ inhibits voltage-dependent Ca2+ channels of airway smooth muscle. Smooth muscle cells were freshly dispersed from pig trachea with collagenase. Depolarization-induced inward Ca2+ currents, measured in whole cell patch-clamp experiments, were inhibited by nifedipine and stimulated by BAY K 8644. Increasing bath Mg2+ from 1 to 21 mM caused a reversible approximately 30% inhibition of current and a positive shift of the peak current-voltage relationship. Voltage-dependent steady-state inactivation had a half-maximal potential (Vh) of -12 mV and a Boltzmann slope factor (k) of 6.0 mV. High Mg2+ caused a positive shift in Vh without affecting k, whereas nifedipine caused a negative shift in Vh and increased k. The inhibition of voltage-dependent Ca2+ channel currents by Mg2+ was quantitatively similar to Mg(2+)-induced relaxation of KCl-contracted tracheal smooth muscle strips. We conclude that inhibition of Ca2+ influx through dihydropyridine-sensitive, voltage-dependent channels by Mg2+ accounts for much of its relaxant action on airway smooth muscle.
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PMID:Role of calcium channel blockade in relaxation of tracheal smooth muscle by extracellular Mg2+. 877 64

The preparation by collagenase dispersion is described of isolated, calcium-tolerant myocytes from the septomarginal (moderator) band dissected from the sheep heart. Cells obtained were small rods (85 x 9 microns), with pronounced striations characteristic of cardiac myocytes. Isolated cells were loaded with the fluorescent ion-sensitive probes Mag-fura-2 or fura-2, for use in microspectrofluorimetry experiments to measure cytosolic free magnesium ([Mg2+]i) and calcium ([Ca2+]i) respectively; cells remained usable for up to 8 h after isolation. Glycolysis and electron transport were inhibited by a short exposure (4 min) to deoxyglucose (15 mM) and cyanide (2 mM), added simultaneously. This appeared to produce a small, but not statistically significant (P = 0.056) rise in [Mg2+]i, presumably resulting from Mg2+ liberated following consumption of MgATP. Inhibition of the Na pump by strophanthidin (20 microM), followed by removal of external Na in the presence of strophanthidin, caused an increase in both [Mg2+]i and [Ca2+]i. The time course of changes in the two ions were dissimilar, so it seems unlikely that the observed rise in the [Mg2+]i was due solely to a direct effect of [Ca2+]i on Mag-fura-2 or due to the displacement of [Mg2+]i by Ca from binding sites. Evidence is presented that suggests sodium-magnesium exchange plays a role in the regulation of myocyte [Mg2+]i.
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PMID:Measurement of intracellular ionized magnesium concentration in myocytes isolated from the septomarginal band of sheep hearts. 884 86

Clostridium sporogenes was isolated from rabbits with antibiotic-associated hemorrhagic diarrhea, then its hemorrhagic toxin was purified from the supernatant by means of hydrophobic interaction chromatography, hydroxyapatite chromatography, and gel filtration. The purified toxin's hemorrhagic activity was completely inhibited by EDTA, but not by PMSF or ovomucoid; and fully restored by the addition of such divalent cations as Zn2+, Ca2+ and Mg2+. The purified toxin did not hydrolyze azocasein, or type I or II collagens. But the purified toxin did hydrolyze type III and IV collagens, and also gelatins prepared from type I, II, III and IV collagens. It appears, therefore that C. sporogenes's toxin is a collagenase that hydrolyzes type III and IV collagens, which are major constituents of the tunica intima and media of blood vessels. And that fact suggests that hemorrhage caused by the toxin depend on its collagenase activity.
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PMID:Purification and some properties of Clostridium sporogenes hemorrhagic toxin. 887 29

Our previous studies have shown that the degree of damage to a liposome corresponds to the variability of the animal species from which the serum comes, and that a complement activating factor (CAF) plays an important role in inducing the activation of the complement system, ultimately leading to the lysis of the liposomes. In this study, our attention focused on the characterization of the bovine serum factor (bCAF) that is involved in complement-mediated immune lysis of the liposome. The active fraction containing CAF partially purified with PEG and ammonium sulfate results in marked activation of the complement system via the alternative pathway when interacted with CAF-depleted serum, whereas the active fraction or CAF-depleted serum alone does not activate the complement. The interaction between lipopolysaccharide (LPS), heparin, zymosan or their mixture in place of CAF and CAF-depleted serum does not result in any significant activation of the complement system. Results from pretreatment with rabbit anti-bovine IgM IgG and rabbit anti-bovine IgG IgG indicate that activation of the complement system is not attributable to the antibody which is generally involved in activation of complement via the classical pathway. The results have further been proven by pretreatment with Concanavalin A (Con A) sepharose and protein G sepharose ruling out the possibility of antibody-mediated activation of complement. Our studies on collagenase and trypsin digestion demonstrate that the relative activity of CAF does not diminish with increase in collagenase concentration, and decreases with increase in trypsin concentration, strongly indicating that CAF does not have a collagen-like domain in its structure. The relative activity of CAF is dramatically inhibited after reduction with 2-mercaptoethanol (2-ME), clearly demonstrating that CAF is sensitive to reduction with 2-ME and confirming a sulhydryl-dependent protein. The optimal activity of CAF is observed in the range of 35-45 degrees C and its half-life at 37 degrees C is about 105 h. Furthermore, the relative activity of CAF increases and gradually approaches a plateau level with the increase of Mg2+ concentration. Obviously, complement activation induced by CAF depends on adequate Mg2+ concentration, confirming that this dependence is characteristic of the alternative pathway.
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PMID:Characterization of bovine serum factor triggering the lysis of liposomes via complement activation. 958 79

Advanced mineralization can cause brittleness of aortic walls with decreased elasticity thereby causing the wall to rupture. Although the precise mechanisms of dystrophic calcification remain unknown, morphological evidence reveals the presence of mineral-associated vesicles in the lesions and defective bioprosthetic valves. In an attempt to demonstrate the calcifiability of the vesicles, small segments of human atherosclerotic aortas with calcified lesions were removed at autopsy and then digested in a crude collagenase solution to release vesicles. A differential centrifugation was then used to isolate calcifiable vesicles, which was precipitated at 300,000 x g for 20 min. An exposure of the vesicles to a calcifying medium containing physiologic levels of Ca2+, Pi, and 1 mM ATP caused Ca deposition in a vesicle protein-concentration dependent manner. The calcifiability of the vesicles was further demonstrated by electron microscopy. Fourier transform spectroscopic analysis of the deposited mineral revealed the presence of a hydroxyapatite phase, closely resembling the native form of mineral in atherosclerotic plaques. In addition, calcifiable vesicles were enriched in ATP-hydrolyzing enzymes including Mg2+ or Ca2+-ATPase and NTP pyrophosphohydrolase that may be involved in normal and pathological calcification. Triton X-100 at 0.01% abolished 80% of both ATPase activity and ATP-initiated calcification. A comparison of vesicles isolated from non-atherosclerotic and atherosclerotic aortas indicated that atherosclerotic vesicles tended to have higher calcifiability. These observations suggest that the calcifiable vesicles play a part in dystrophic calcification of aortas in atherosclerosis.
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PMID:Isolation of calcifiable vesicles from human atherosclerotic aortas. 1021 64

Magnesium (Mg) inhibits the influx of calcium in vascular smooth muscle cells. The purposes of this study were to test the hypothesis that an intravenous administration of magnesium might effect the complement response and to determine the effects of a magnesium pretreatment of patients with acute myocardial infarction (AMI) on the incidence of reperfusion injuries. Thirty-eight AMI patients were treated with coronary reperfusion therapy within 6 hours of onset. They were randomly divided into two groups: group pretreated with intravenous magnesium sulfate (0.27 mmol/kg) (magnesium group, n = 19), and nonpretreated controls (placebo group). The reperfusion injuries observed within 1 hour after the coronary reperfusion included arrhythmias, aggravated chest pain, and ST segment elevation in 12-lead electrocardiograms. Coronary recanalization was performed in 36 patients. The incidence of reperfusion arrhythmia was significantly lower in the magnesium group than in the placebo group (17% vs 78%, p<0.001). At the postreperfusion stage, there was a tendency for the degree of ST segment reelevation in the magnesium group lower than in the placebo group (2.5 +/- 2.3 mm vs 4.7 +/- 3.8 mm, p = 0.07). No marked difference was observed in the incidence of chest pain aggravation between the two groups (67% vs 73%, ns). The peak serum levels of interleukin-6 (IL-6) were significantly lower in the magnesium group than those in the placebo group (38.9 +/- 25.0 vs 92.3 +/- 76.5 pg/mL, p = 0.016). The peak serum levels of matrix metalloproteinase-1 (MMP-1) were lower than those in the placebo group (16.2 +/- 4.8 vs 19.7 +/- 9.0 ng/mL, p = 0.09), but the difference was not significant. A positive correlation was observed between the peak MMP-1 values and the peak IL-6 values (r = 0.57, p = 0.001) in all patients. Increased serum ionized Mg2+ may inhibit arrhythmic recurrence and the production of IL-6 and MMP-1 after reperfusion and prevent the increase of myocardial lesions caused by calcium overload on myocytes. The increased IL-6 production may induce MMP-1, leading to tissue organ injury. Pretreatment with magnesium sulfate may protect the myocardium of AMI patients from reperfusion injuries.
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PMID:Effect of magnesium sulfate pretreatment and significance of matrix metalloproteinase-1 and interleukin-6 levels in coronary reperfusion therapy for patients with acute myocardial infarction. 1043 97


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