Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.15.1 (ACE)
 18,300 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A morphologic and growth control variant of bovine aortal endothelial cells has been isolated and shown to synthesise factor VIII antigen (McAuslan and Reilly '79). The variant also possesses the endothelial surface markers angiotensin converting enzyme and alpha 2-microglobulin. The normal cell synthesises fibronectin and deposits it underneath the cells; the variant also synthesises fibronectin. At least three times more fibronectin is distributed over the upper cell surface of variants. This correlates with the three-fold increased binding of the replication inhibitor Con A and suggests a role of fibronectin in endothelial cell growth control. When stimulated to migrate by CuII ions, the variant leaves deposits of fibronectin in its trail; in contrast, migrating normal cells do not, but they do redistribute their surface fibronectin. As revealed by scanning electron microscopy, variant cells are unusual in that they grow over or under cultured normal endothelial cells. It is proposed that during the process of neovascularisation, variant cells have a special function as lead cells that lay down fibronectin on which an endothelium can become established.
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PMID:Variant endothelial cells. Fibronectin as a transducer of signals for migration and neovascularisation. 615 98

Several enzymes, enzyme inhibitors, receptors and transport structures are situated on the luminal surface of endothelium. Some enzymes and transport systems are continuously active and, in effect, regulate the composition of blood moving downstream. Other components are latent. Their activities are not expressed in the absence of stimulus. Thus, endothelial cells injured by granulocytes or viral infection possess receptors for the Fc segment of IgG and for C3b, whereas normal endothelial cells do not. Both normal and injured endothelial cells express receptors for Clq. To visualize surface enzymes, inhibitors, receptors and transport structures, we have prepared surface replicas suitable for high resolution EM. The surface replication technique, coupled with immunocytochemical procedures, facilitates studies of the topographies of surface enzymes such as angiotensin converting enzyme (ACE) and carboxypeptidase N (CPN). In addition, the replicas provide unique views of the glycocalyx, a cell coating previously believed to be amorphous but now seen to be a highly organized carpet-work under which surface enzymes, receptors, etc are embedded. Given its content of fibronectin, the glycocalyx may be the Clq receptor. Cells treated with antibodies to ACE or CPN show disarrayed glycocalyces and bind Fc and C3b. Latency of the Fc and C3b receptors may be owing to the physical barrier provided by the glycocalyx. Apparently, damage to the glycocalyx creates conditions favoring binding of immune complexes, complement activation and intravascular coagulation with loss of gradients between blood and parenchyma. Whether some non-thrombogenic properties of endothelium require an intact glycocalyx deserves consideration as does the role of the glycocalyx in regulating microvascular permeability.
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PMID:The ultrastructural basis of endothelial cell surface functions. 646 85

To provide an in vitro system for studying retinal capillary function we have developed methods for isolation and culture of microvascular endothelial cells from retina. Retinal microvessels were isolated by homogenization of the retina and collection of the microvessels onto nylon mesh. Treatment of the isolated microvessels with collagenase and dispase followed by Percoll gradient centrifugation yielded endothelial cells that were largely free of pericytes. A homogeneous population of endothelial cells that were capable of at least six population doublings was obtained by plating onto a fibronectin coated substrate in plasma derived serum. The endothelial origin of these cells was confirmed by the presence of Factor VIII antigen, angiotensin converting enzyme activity, numerous tight junctions, and a cell surface that did not bind platelets. A second cell type, which did not exhibit these cell markers and which is presumably the intramural pericyte, was obtained when the isolated microvessels were plated on tissue culture grade plastic in fetal bovine serum.
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PMID:Primary culture of microvascular endothelial cells from bovine retina: selective growth using fibronectin coated substrate and plasma derived serum. 714 46

Hypertension induced in rats by suprarenal banding has a blood pressure elevating effect that is accompanied by the occurrence of cardiac hypertrophy and fibrosis. This phenomenon is already present at 2 weeks after banding and persists up to 1.5 years. The increase in cardiac weight is mostly due to the development of fibrosis, since myocytes are only slightly increased in size. The fibrotic tissue consists mainly of fibronectin and collagen and contains numerous cellular elements. The occurrence of fibrosis can be completely inhibited by the administration of the specific ACE inhibiting drug, ramipril, which indicated that angiotensin II may directly stimulate fibroblasts to produce fibronectin and collagen. The antifibrotic effect of ramipril was also present in a low dosage that did not lower blood pressure, confirming the hypothesis that angiotensin II has a direct effect on connective tissue cells and their ability to produce extracellular matrix proteins. The direct effect of the renin-angiotensin system on the activity of interstitial cells was further proven by molecular biology techniques showing an upregulation of transcription for collagen I and III which is prevented by ACE inhibition.
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PMID:Extracellular matrix deposition in hypertensive hearts antifibrotic effects of ramipril. 755 70

In genetic and acquired hypertension, a structural remodeling of the nonmyocyte compartment of myocardium, including the accumulation of fibrillar collagen and other components of the extracellular matrix (ECM) within the interstitium, represents a determinant of pathologic hypertrophy that leads to ventricular dysfunction. Therefore, to evaluate the potential benefit of the angiotensin converting enzyme (ACE) inhibitor quinapril in reversing the interstitial remodeling in spontaneously hypertensive rats (SHR) with established left ventricular hypertrophy (LVH), we treated 16-week-old male SHR with oral quinapril (average dose, 10 mg/kg body weight/day) for 20 weeks. Interstitial fibrosis was determined morphometrically using an automatic image analyzer. The amount of collagen was evaluated by measuring myocardial hydroxyproline concentration. Myocardial deposition of collagen molecules (types I, III, and IV) and other ECM components (fibronectin, laminin) was analyzed by immunohistochemical techniques using specific monoclonal antibodies. The activity of ACE was measured in left ventricular tissue by a fluorometric assay. In quinapril-treated SHR compared with 36-week-old untreated SHR and age- and sex-matched Wistar-Kyoto (WKY) controls, we found 1) a lesser degree of LVH and a lesser level of blood pressure, 2) a lesser degree of interstitial fibrosis, represented by less interstitial collagen volume fraction (5.73 +/- 0.45% v 3.42 +/- 0.28%, P < .05; WKY, 3.44 +/- 0.66%), 3) a lower hydroxyproline concentration (1.09 +/- 0.05 mumol/L/g dry weight/100 g body weight to 0.81 +/- 0.05 mumol/L/g dry weight/100 g body weight, P < .05; WKY, 0.96 +/- 0.06 mumol/L/g dry weight/100 g body weight), 4) a lesser presence of collagen fibers, and 5) a lesser presence of collagen IV, fibronectin, and laminin.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Quinapril decreases myocardial accumulation of extracellular matrix components in spontaneously hypertensive rats. 757 98

A group of 17 patients with ischemic heart disease, significant left ventricular dilatation and congestive heart failure, class III NYHA (9 patients) and class IV NYHA (8 patients) was studied. The patients received angiotensin converting enzyme inhibitor--captopril 75 mg/day or perindopril 4 mg/day--added to diuretics, digitalis and nitrates. The plasmatic level of fibronectin was investigated, by radial immunodiffusion, before and one month after the beginning of the treatment with angiotensin converting enzyme (ACE) inhibitor. The plasmatic level of fibronectin is increased significantly (p < 0.001) while the cardiothoracic ratio is decreased significantly (p < 0.02) after one month of ACE inhibitors treatment. A positive correlation between the increase of the plasmatic level of fibronectin and the decrease of cardiothoracic ratio is found (r = 0.62; p < 0.01). The increased fibronectin plasmatic level can be a marker of the favorable effect of ACE inhibitor on the myocardium interstitium.
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PMID:Correlation between fibronectin and cardiothoracic ratio in heart failure treated with angiotensin converting enzyme inhibitors. 761 96

The in vivo effects of alacepril (1-[(S)-3-acetylthio-2-methylpropanoyl]- L-prolyl-L-phenylalanine), an angiotensin converting enzyme inhibitor, and SC-52458 (5-[(3,5-dibutyl-1H-1,2,4-triazol-1- yl)methyl]-2-[2-(1H-tetrazol-5-ylphenyl)]pyridine), an angiotensin AT1 receptor antagonist, were examined on the cardiac and aortic gene expressions of extracellular matrices and TGF-beta 1 in young spontaneously hypertensive rats (SHR). In SHR, types I and III collagen mRNAs were increased in the left ventricle, and in contrast, fibronectin, collagen IV, and transforming growth factor-beta 1 (TGF-beta 1) mRNAs were increased in aorta, compared with those in Wistar-Kyoto rats. All the enhanced mRNAs in both organs in SHR were significantly inhibited by the short-term treatment with the above two drugs. Thus, angiotensin AT1 receptor may play an important role in the regulation of extracellular matrices and TGF-beta 1 expressions in SHR.
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PMID:Role of angiotensin II in extracellular matrix and transforming growth factor-beta 1 expression in hypertensive rats. 782 53

Plasma fibronectin (FBN) and angiotensin I-converting enzyme (ACE) were prospectively measured in 50 burn patients from the day of admission to day 28 after the trauma with the aim of finding biochemical markers of pulmonary injury by smoke inhalation. Patients were divided into three groups on the basis of fiberoptic bronchoscopy results (group I: healthy lungs; group II: burned lungs; group III: infected lungs). A decrease in FBN concentrations was observed in the three groups but was larger in group II than in the other groups, especially at day 2 (P < 0.05). A similar profile was observed for plasma ACE activity. Factors other than lung injury may influence plasma FBN and ACE levels, in particular the burned body surface area, an acute event such as septicemia, or outcome. However, repeated measurements of both markers could help in the assessment of lung injury in the follow-up of burn patients.
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PMID:Plasma fibronectin and angiotensin-converting enzyme: markers of primary pulmonary injury in burn patients. 795 10

This review compares the clinical usefulness of immunological methods for the detection of structural components and metabolites of bacteria and fungi. Bacterial antigens (especially those of Mycobacterium, Neisseria, Staphylococcus aureus, Yersinia enterocolitica, Escherichia coli, Salmonella, Chlamydia, and Brucella) are best detected by enzyme-linked immunosorbent assay. Methods involving antibodies are more expensive and are effective only when performed in series. The detection of antibodies that recognize S aureus teichoic acid merely confirms the presence of a metastatic complication. Tissue invasion by Candida albicans is not yet reliably detectable by the presence of a specific antigen. Simple, but not completely reliable methods are available such as the latex test for mannans detection and/or agglutination with liposomes for detecting 48-kDa cytoplasmic protein antigen and an assay for detecting enolase antigen. A latex agglutination test has also been developed for the mannans antigen of Aspergillus and for Cryptococcus neoformans capsular polysaccharide; the latter test is more cost effective. The sensitivity of both tests is improved by serial assays. A negative finding with hemagglutination-based antibody tests rules out C albicans infection, and titers of 1/640 or higher have been associated with disseminated infection by Aspergillus. Concentrations of C albicans blastopore antigen antibodies higher than 400 IU/ml can be seen in disseminated candidiasis. High concentrations of endotoxin are indicative of imminent septic shock. Some biological indicators (C reactive protein, angiotensin converting enzyme, fibronectin, elastase-alpha 1-antitrypsin complex, tumor necrosis factor and interleukin-6) have been used to rule out a bacterial cause of fever.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Immunological methods for the detection of structural components and metabolites of bacteria and fungi in blood. 821 14

We studied the effect of the angiotensin converting enzyme (ACE) inhibitor, quinapril, on the clinical and morphological lesions of a normotensive model of immune complex nephritis. Untreated rats developed massive nephrotic syndrome, intense cell proliferation and glomerular and tubulointerstitial lesions. In the renal cortex of nephritic rats there was a significant increase in gene expression of TGF-beta 1, fibronectin and collagens, and ACE activity. Systolic blood pressure remained normal with progression of the disease. Administration of quinapril for three weeks to animals with glomerular lesions (proteinuria 20 to 50 mg/day) avoided the development of intense proteinuria (79 +/- 28 vs. 589 +/- 73 mg/day, P < 0.001) and decreased cell proliferation, glomerulosclerosis, tubulointerstitial lesions, and inflammatory infiltrates. Cortical gene expression of TGF-beta 1 and matrix proteins was also diminished. ACE activity was inhibited by 68% in renal cortex. These results show that quinapril administration to normotensive rats with immune complex nephritis decreases proteinuria and glomerular and tubulointerstitial lesions, probably modulating the local angiotensin II generation and its effects on cell growth, TGF beta and matrix protein synthesis.
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PMID:ACE inhibition reduces proteinuria, glomerular lesions and extracellular matrix production in a normotensive rat model of immune complex nephritis. 858 37


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