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)

Endothelial cells from human umbilical veins were isolated by collagenase treatment. Cells were cultured in the presence of either 20% fetal bovine serum (FBS) or 20% human serum (HS). At confluency, endothelial cell lipids were labeled with tracer concentrations of tritiated arachidonic acid, then extracted and separated into lipid subclasses by thin layer chromatography. The fatty acid composition of each lipid class was determined by glass capillary gas-liquid chromatography analysis and compared to that of cells freshly isolated from the cord (NC cells). The fatty acid compositions differed only in phospholipids. Polyunsaturated fatty acids (PFAs), arachidonic, and linoleic acids were depleted in FBS cell phospholipids and replaced by both stearic and oleic acids. No significant difference could be observed between NC cell and HS cell phospholipids. We conclude that PFAs might be decreased in FBS cells because of the relative paucity of PFAs in FBS as compared to HS. It seems therefore more convenient to cultivate endothelial cells in the presence of HS, especially in respect to their phospholipid content of arachidonic acid, which is the physiological reservoir for prostacyclin synthesis.
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PMID:Fatty acid composition in native and cultured human endothelial cells. 669 71

The use of human omentum as an alternative to veins as a source of cells for seeding onto small-caliber vascular prostheses has awakened controversy as to the identification of the predominant cell type derived from this source. Mesothelial cells from omentum were extracted by collagenase digestion, and cultured until a monolayer was formed. These cells showed positivity for monoclonal antibodies specific for endothelial cells (anti-CD34 QBEND10), antibodies to intermediate filaments (anti-vimentin and anti-desmin) and anti-smooth muscle cell antibodies (anti-actin and anti-total actin). The mesothelial cells behaved like endothelial cells derived from vein when seeded onto polytetrafluoroethylene prostheses, showing high levels of prostacyclin production. This report provides additional evidence of the non-endothelial origin of the cells derived from human omentum.
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PMID:Coatings for vascular prostheses: mesothelial cells express specific markers for muscle cells and have biological activity similar to that of endothelial cells. 755 50

One hundred and eleven mongrel dogs were used for this study. Endothelial cells were harvested from jugular vein or omentum with methods of collagenase digestion and density gradient separation. Animal model of prosthetic interposition into the inferior vena cava with or without distal arteriovenous fistula was established. The complete endothelialization was established 5 to 10 days following a high density seeding. The neointimal hyperplasia was inhibited. A 100-day 100% patency of prosthesis was reached. The seeded endothelium secreted higher level of PGI2 than normal control and lower level of TXB2, hence the positive effect of distal AVF functioning for a week on the patency was demonstrated. This method used in 10 cases with Budd-Chiari syndrome resulting in good outcome after 3 to 5 years follow-up. We conclude that the endothelial seeding technique has a promising future using in the venous circuit.
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PMID:[Experimental study and clinical application of endothelium seeded vena caval prostheses]. 784 98

Individual prostanoids have distinct potencies in activating intracellular signaling pathways and regulating gene expression in osteoblastic cells. The E-series prostaglandins (PGs) are known to stimulate matrix metalloproteinase-1 (MMP-1) synthesis and secretion in certain rodent and human osteoblastic cells, yet the intracellular events involved remain unclear. To further characterize this response and its signal transduction pathway(s), we examined prostanoid-induced expression of the MMP-1 gene in the rat osteoblastic osteosarcoma cell line UMR 106-01. Northern blot analysis demonstrated that prostaglandin E2 (PGE2) and PGE1 were very potent stimulators (40-fold) of MMP-1 transcript abundance, PGF2 alpha and prostacyclin were weak stimulators (4-fold), and thromboxane-B2 had no effect. The marked increase in MMP-1 transcript abundance after PGE2 treatment was first detected at 2 h, became maximal at 4 h, and persisted beyond 24 h. This response was dose dependent and elicited maximal and half-maximal effects with concentrations of 10(-6) and 0.6 x 10(-7) M, respectively. Cycloheximide, a protein synthesis inhibitor, completely blocked this effect of PGE2, suggesting that the expression of other genes is required. Nuclear run-on experiments demonstrated that PGE2 rapidly activates MMP-1 gene transcription, with a maximal increase at 2-4 h. The second messenger analog, 8-bromo-cAMP, mimicked the effects of PGE2 by stimulating a dose-dependent increase in MMP-1 messenger RNA (mRNA) levels, with a maximal effect quantitatively similar to that observed with PGE2. Thus, in UMR 106-01 cells, different prostanoids have distinct potencies in stimulating MMP-1 mRNA abundance. Our data suggest that PGE2 stimulation of MMP-1 synthesis is due to activation of MMP-1 gene transcription and a subsequent marked increase in MMP-1 mRNA abundance. This effect is dependent on de novo protein synthesis and is mimicked by protein kinase-A activation.
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PMID:Prostanoid-induced expression of matrix metalloproteinase-1 messenger ribonucleic acid in rat osteosarcoma cells. 792 6

Blood vessel angiogenesis is an important component of chronic synovitis, and its regulation may be mediated through local production and effects of certain inflammatory cytokines, including interleukin-1 (IL-1). Retinoic acid (RA) can alter the progression of some inflammatory arthritic diseases, presumably through effects on fibroblast collagenase and PGE2 production. To explore alternate hypotheses, we examined the interaction of retinoic acid and IL-1 on endothelial cell (EC) function and found that RA directly affects and modifies the effects of IL-1 on EC proliferation, prostacyclin production, and plasminogen activator inhibitor capacity (PAI-1). With respect to EC proliferation, cis- and trans-retinoic acid and retinol induced a dose-dependent increase of [3H]TdR uptake by cultured ECs, independent of the effects of serum or eicosanoid production. This effect was blocked by IL-1. With respect to EC prostacyclin production, although retinoic acid alone had no effect, cis and trans-retinoic acid and retinol all induced a dose-dependent increase in IL-1-mediated prostacyclin production, which was most marked at higher concentrations (20 U/ml) of IL-1. This effect was mediated through effects independent of cyclooxygenase (COX) production. With respect to plasminogen activator inhibitor capacity, both IL-1 and retinoic acid stimulated EC PAI-1 synthesis, but the individual effects were additive, with RA augmenting the known IL-1 effects on EC PAI-1 production. The interaction between RA and IL-1 on the endothelium, described in this study, may play a role in the fashion through which retinoic acid alters the expression of synovitis in certain types of experimental inflammatory arthritis.
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PMID:Retinoic acid effects on endothelial cell function: interaction with interleukin 1. 802 Jan 93

The aim of the study was to investigate the effect of aging on cytoprotective properties of prostaglandins. Hepatocytes were obtained by collagenase perfusion of livers of young (4-6 mo) and old (24-28 mo) male Wistar rats. Cells were incubated for 1.5 h in Krebs-Ringer-bicarbonate buffer containing glucose and 3H-leucine in the presence of galactosamine (2.5-100 mM), PGE1, or two prostacyclin analogues: 9 beta-methylcarbacyclin and TRK-100. Cell damage was assessed by decrease in the rate of protein synthesis measured as 3H-leucine incorporation into acid precipitable material, and by increase in lactate dehydrogenase release into the medium. Hepatocytes from old rats were more susceptible to suppression of protein synthesis by GalN than cells of young ones. Preincubation of cells for 15 min with 9MC (41-560 nM) or PGE1 (10-100 nM), but not with TRK-100, before adding 10 mM GalN, led to a partial recovery of protein synthesis in both age groups. GalN increased LDH release and decreased ATP/ADP ratio to a similar extent in hepatocytes of young and old rats; both parameters were not altered by preincubation of cells with PGs. PGE1 and 9MC, but not TRK-100, elevated cyclic AMP content in hepatocytes of young but not old rats. Glucagon and forskolin similarly increased cyclic AMP content in cells of both young and old animals. These in vitro results suggest that PGE1 and some prostacyclin analogues might protect hepatocytes of both young and old rats from chemical damage, and stress the necessity for further research on cyto- and hepato-protection in the elderly.
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PMID:Prostaglandin cytoprotection of galactosamine-incubated hepatocytes isolated from young and old rats. 803 Aug 38

This study examined the influence of dietary essential fatty acids on the cooperativity of isolated adipocytes and stromal-vascular cells in the biosynthesis of prostaglandins. Sprague-Dawley rats were fed either a diet rich in essential fatty acids (20% corn oil) or a diet poor in essential fatty acids (20% tallow) for 4 wk. Preparations containing primarily adipose cells (adipocytes) or stromal-vascular cells (nonfat cells) were obtained from epididymal fat pads by collagenase digestion and repeatedly washed. Prostaglandin production was evaluated in basal and epinephrine-stimulated media after incubation with either adipocytes or adipocytes+nonfat cells. Prostaglandin E2 and prostacyclin production by adipocytes+nonfat cells was dose-dependent with epinephrine stimulation in cells from rats fed both diets. Both prostaglandin E2 and glycerol release in response to epinephrine (10-100 mumol/L) stimulation from adipocytes or from adipocytes+nonfat cells were significantly higher for cells from corn oil-fed rats than for cells from tallow-fed rats. Regardless of dietary treatment, epinephrine-stimulated prostaglandin E2 and prostacyclin release from adipocytes+nonfat cells was much greater than from adipocytes. These results suggest that a diet high in essential fatty acids precipitates a higher prostaglandin E2 secretion and that nonfat cells potentiate the secretion of prostaglandin E2 and prostacyclin by adipocytes regardless of diet.
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PMID:The cooperation of adipocytes and stromal cells in the secretion of prostaglandins by rat adipose tissue is not influenced by diet. 832 May 61

During pregnancy, the uterine artery demonstrates refractoriness to vasoconstriction by infused angiotensin II (AII). AII increases prostacyclin (PGI2) production by uterine artery endothelium from pregnant ewes, and this response is mediated via the AT1 receptor (AT1-R). This response is also unique to pregnancy because AII does not stimulate PGI2 production by uterine artery endothelium from nonpregnant ewes. We therefore hypothesize that the increase in uterine artery PGI2 production in response to AII in pregnancy is associated in part with a concomitant increase in AT1-R expression in uterine artery endothelium. Endothelium-derived protein was directly removed from the lumenal surface of freshly isolated uterine and systemic (omental) arteries from nonpregnant and pregnant ewes. AT1-R expression was then measured in both the endothelium-derived fraction and endothelium-denuded vascular smooth muscle (VSM) fraction by Western analysis. AT1-R was detected as 54- and 65-kDa proteins in all samples, as well as adrenal cortex control. AT1-R expression increased more than 8-fold in uterine artery endothelium of pregnant ewes over that in nonpregnant ewes at each of four gestational ages (P < 0.05 at 110, 120, 130, 142 days, n = 4 each vs. n = 6 nonpregnant). No significant differences were seen, however, from 110 to 142 days of gestation. In contrast, whereas the level of AT1-R staining in omental artery endothelium in nonpregnant ewes was higher than in uterine artery, AT1-R increased less in pregnant ewes (2-fold) and only reached significance over nonpregnant values at 110 and 120 days, or when data was combined irrespective of gestational age (P < 0.05). Although AT1-R was also detected in uterine and omental artery VSM, little or no change in expression was observed in pregnancy. Results were confirmed by immunohistochemical staining of arterial cross sections, and the increase in AT1-R expression in uterine artery endothelium was confirmed by RT/PCR amplification of AT1-R messenger RNA from collagenase dispersed cells (n = 4 pregnant vs. n = 4 nonpregnant, mean 20-fold increase, P < 0.028). We conclude that increased uterine artery endothelial PGI2 responsiveness to AII during pregnancy is indeed associated with a correspondingly marked and localized increase in expression of the endothelial AT1-R receptor. We believe our findings allow a more detailed understanding of the molecular mechanisms that underlie increased uterine blood flow that is so central to the normal development of the growing fetus, and on dysfunction may lead to conditions such as preeclampsia.
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PMID:Pregnancy induces an increase in angiotensin II type-1 receptor expression in uterine but not systemic artery endothelium. 897 39

During normal pregnancy, and especially in the third trimester, both uterine blood flow and prostacyclin production by ovine uterine arteries are dramatically increased. We sought to determine if this is due, in part, to an increase in cyclooxygenase (COX) expression in the uterine artery endothelium. In this study we compared COX expression in uterine artery endothelium from nonpregnant and third-trimester pregnant (110-142 days' gestation) ewes. COX-2 expression was not detectable by Western blotting in uterine artery endothelium or vascular smooth muscle (VSM). In contrast, COX-1 expression was clearly observed in uterine artery. Immunohistochemical localization of COX-1 was endothelium > VSM, with both cell types showing an increase in COX-1 during the third trimester of pregnancy. COX-1 protein and messenger RNA (mRNA) levels were also detectable in collagenase dispersed endothelial cells, with expression of COX-1 in uterine artery endothelial cells dramatically increased during the third trimester of pregnancy at both the level of protein (346.4 +/- 28% of nonpregnant controls, P < 0.0005) and mRNA (51.04 +/- 7.98-fold of nonpregnant controls, P < 0.001). We conclude that the pregnancy-induced increases in prostacyclin production by uterine arteries is largely due to a dramatic increase in expression of COX-1 mRNA and associated protein predominantly occurring in the uterine artery endothelium and, to a lesser extent, in the VSM.
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PMID:Pregnancy increases ovine uterine artery endothelial cyclooxygenase-1 expression. 944 51

The search for a noncalcifying tissue material to be used for valve replacement application continues to be a field of extensive investigation. A series of porcine pericardial membranes was prepared by modifying the glutaraldehyde--treated tissues with albumin and subsequently immobilizing bioactive molecules like PGE1, PGI2 or heparin via the carbodiimide functionalities. The in vitro calcification and collagenase degradation of these modified tissues were studied as a function of exposure time. Furthermore, the biocompatibility aspects of such novel interfaces were established by platelet adhesion and fibrinogen adsorption. The results reported in this article propose that the treatment with antiplatelet agents such as albumin, heparin and prostaglandins (PGE1 or PGI2) change the surface conditioning of pericardial tissues, suggesting a possible role of deposited serum components in affecting mineralization process on bioprosthesis. Therefore, it is worthy to hypothesize that besides inhibiting the accumulation of calcium in the devitalized cells, the early formation of a conditioning layer on the bioprosthesis surface may affect salt precipitations, determining the propensity of the implant to calcify. More detailed studies are needed to understand the involvement of plasma proteins and cellular components of the recipient blood in tissue-associated calcification.
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PMID:Surface-immobilized biomolecules on albumin modified porcine pericardium for preventing thrombosis and calcification. 1053 11


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