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

Lung involvement was studied by perfusion scan, ventilation scan, pulmonary clearance rate of 99mTc DTPA and pulmonary function tests in 20 patients with systemic sclerosis (SSc). Decreased plasma angiotensin converting enzyme (ACE) activity and increased levels of von Willebrand Factor Antigen (vWF:Ag) were found in all patients with SSc. The relationship between ACE levels and lung involvement was not statistically significant, however levels of vWF:Ag correlated with parameters of lung vascular alterations. An inverse relationship between the reduced ACE levels and ESR was found. It is likely that ACE levels reflect the inflammatory aspect of the disease. Further studies of ACE synthesis, release and inhibition are needed to determine the mechanism of the observed decreased activity in SSc.
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PMID:Clinical correlations of plasma angiotensin converting enzyme (ACE) activity in systemic sclerosis: a longitudinal study of plasma ACE level, endothelial injury and lung involvement. 217 47

A reliable technique to produce consistently pure cultures of endothelial cells prepared from isolated rat brain capillaries has been established. The cells express many of the morphological and antigenic characteristics of endothelium in vivo, including the formation of tight junctions and possession of Factor VIII/von Willebrand Factor antigen (FVIII/vWF) and angiotensin converting enzyme (ACE). Using indirect immunofluorescence, surface IgG Fc receptors (FcR) could not be demonstrated, either when the cells were incubated in aggregated IgG, or in adult rat serum. Rat peritoneal macrophages served as a positive control. However, permeabilization of the endothelial cells with glacial acetic acid/ethanol prior to incubation with IgG allowed the demonstration of internal binding sites. The lack of surface receptors in the normal state does not rule out the possibility of their induction during pathological conditions.
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PMID:Brain capillary endothelial cells in vitro lack surface IgG Fc receptors. 294 4

The placental endothelium contributes to regulating transplacental exchange and maintaining the immunological maternofetal barrier. We characterized the endothelial phenotype in human normal term placentae with a panel of antibodies to endothelial antigens using a standardized immunofluorescence method. Placental endothelium strongly expressed vWF, PAL-E, H-antigen, thrombomodulin, PECAM-1, CD34, CD36, ICAM-1, CD44, thy-1, A10/33-1, VE-cadherin, caveolin-1 and HLA-G, whereas occludin, claudin-1, eNOS, angiotensin converting enzyme (ACE), ICAM-2, endoglin and integrin-alphathetabeta(3)were weakly expressed. PGI(2)synthase, tissue factor, E-selectin and VCAM-1 were not detected. Some antigens were heterogenously expressed along the vascular tree or within individual villi. Expression of ACE, eNOS, vWF, P-selectin, E-selectin, integrin alpha(v)beta(3)and endoglin was stronger in the maternal decidual vessels, while PECAM-1, CD44, thy-1 and caveolin-1 expression was stronger in fetal vessels. Some endothelial markers were present in trophoblasts and stroma. Endothelial proliferation was apparent in mature intermediate and terminal villi. There was limited inflammatory response to TNFalpha in explants, characterized by upregulation of vWF, P-selectin, PECAM-1 and CD44, downregulation of thrombomodulin, but no increase in ICAM-1 expression, nor induction of E-selectin, VCAM-1 or tissue factor. These patterns of heterogeneity, proliferative activity and inflammatory activation may underlie the specific physiological roles of the placental endothelium.
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PMID:Phenotype of the endothelium in the human term placenta. 1116 50

In June, 1997, we initiated a prospective study to analyze the effect of granulocyte colony-stimulating factor (G-CSF) on coagulation system in peripheral blood stem cells (PBSC) donors following G-CSF administration. Since, 25 consecutively healthy donors received G-CSF (filgrastim) to mobilize and collect PBSC and 20 donors were finally included in the study. Blood samples were collected immediately before starting G-CSF and prior to PBSC collection to analyze the following parameters: prothrombin time (PT), activated partial thromboplastin time (APTT), fibrinogen, hypercoagulability markers (D-dimer, TAT complex, F1 + 2), natural anticoagulants (antithrombin, protein C, protein S), endothelial activation markers [von Willebrand factor antigen (vWF:Ag) and angiotensin converting enzyme (ACE)], and resistance to activated protein C. We found a significant increase in F1 + 2 and D-dimer while a significant decrease of antithrombin and protein C activity was evidenced. Regarding endothelial cell activation markers, a significant increase of vWF:Ag with a slightly significant decrease of ACE were also observed. Therefore, in PBSC donors receiving G-CSF our results reveal activation of both coagulation and endothelial cells that could favor the developing of thrombotic events. In consequence, a careful monitoring should be considered in those cases with risk factors for thrombosis.
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PMID:Induction of a hypercoagulability state and endothelial cell activation by granulocyte colony-stimulating factor in peripheral blood stem cell donors. 1220 56

IgA nephropathy is currently the most frequently occurring type of primary glomerulonephritis. Studies aimed at determining the factors of favorable and unfavorable prognosis in the progression of the disease are conducted. Apart from the above renal disease progression factors, it seems that renal functional reserve (RFR), indirectly indicating the functional status of intrarenal vessels can be a marker assisting in determining prognosis and effectiveness of applied treatment. Decrease in RFR is one of the first symptoms of renal damage, since it precedes decrease in GFR assessed in resting condition. The aim of our study was to assess selected functional (RFR), metabolic, and genetic parameters of renal disease progression in patients with IgA nephropathy, as well as to determine their effect on clinical progression of the disease. Material and methods. The study comprised 30 patients with renal biopsy proven IgA nephropathy, aged 35,2 +/- 8,9, 12 women and 18 men, who had conducted a 12-month period of observation and treatment. The patients' RFR was measured and the following parameters in blood pressure samples were established: creatinine, BUN, uric acid, total cholesterol (TCH), HDL and LDL and TG, homocysteine, endothelium functional indicators: vWF:Ag, TPA:Ag, PAI-1, polymorphism of the human angiotensin converting enzyme gene and endothelial nitric oxide synthase gene. In 24-hour urine collection N-acetylglucosaminidase excretion and daily protein loss were measured. Results. During treatment, changes in some biochemical indicators were observed (uric acid, TCH, LDL, DUB, NAG, erythrocyturia, homocysteine), while others remained stable. Statistically significant differences in concentrations of endothelial antigens: vWF:Ag and PAI-1 were found. Conclusions. Based on the analysis of the results it was concluded that functional status of intrarenal vessels is related to functional status of endothelium and renal tubulae, and also that it probably affects the response to treatment. Decrease of proteinuria during treatment is, among others, related to decrease of metabolic disorders, while the initial results of analysis of polymorphism of the human angiotensin converting enzyme gene and endothelial nitric oxide synthase gene suggest that it may affect the decrease of proteinuria and concentration of homocysteine in the blood.
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PMID:[Some metabolic and genetic risk factors and the progression of IgA nephropathy--preliminary report]. 1714 95

Single-gene disorders explain only a minority of stroke cases. Stroke represents a complex trait, which is usually assumed to be polygenic. On this topic, the role of a wide number of candidate genes has been investigated in stroke through association studies, with controversial results. Therefore, it is difficult for the clinician to establish the validity and the level of clinical applicability of the previously reported associations between genetic factors and stroke. This review is an update and an extensive analysis of the more recent association studies conducted in stroke. We evaluated a number of studies on several candidate genes (including F5, F2, FGA/FGB/FGG, F7, F13A1, vWF, F12, SERPINE1, ITGB3/PLA1/PLA2/ITGA2B, ITGA2, GP1BA, ACE, AGT, NOS3, APOE, LPL, PON1, PDE4D, ALOX5AP, MTHFR, MTR, and CBS), providing a final panel of genes and molecular variants. We categorized this panel in relation to the degree of association with stroke, supported by the results of meta-analyses and case-control studies. Our findings could represent a useful tool to address further molecular investigations and to realize more detailed meta-analyses.
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PMID:Genetic polymorphisms for the study of multifactorial stroke. 1842 1