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 protective role against atherosclerosis can be attributed to angiotensin converting enzyme inhibitors (ACE-I), since they have been shown to reduce mortality in patients at cardiovascular risk. Since plasma levels of adhesion molecules are considered surrogate markers of endothelial cell activation and atherogenesis, we compared the levels of adhesion molecules after treatment with the ACE-I enalapril or the direct angiotensin- receptor antagonist losartan or placebo. In a randomized, controlled trial, 21 hypercholesterolemic volunteers received 50 mg/d losartan or 20 mg/d enalapril or placebo for twelve weeks. Plasma levels of circulating intercellular adhesion molecule-1 (cICAM-1), vascular adhesion molecule-1 (cVCAM-1), and E-selectin (cE-SEL) were measured by ELISA. Surface expression of ICAM-1 on circulating leukocytes was determined by flow cytometry. Enalapril and losartan but not placebo induced a small but stable decrease of cICAM-1 and cVCAM-1, while cE-SEL and leukocyte expression of ICAM-1 remained unchanged. The lowering of plasma adhesion molecules may indicate an antiatherogenic effect of angiotensin II blockade in hypercholesterolemia. While such preventive effect will have to be proven in clinical trials, our results do not support a preference for either enalapril or losartan with regard to their possible vasoprotective role.
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PMID:Angiotensin receptor blockade decreases markers of vascular inflammation. 1547 31

Adrenomedullin (AM), an ubiquitous regulatory peptide with different actions, is known to be elevated in different clinical situations, including diabetes mellitus (DM), but its potential role in the pathogenesis of diabetic vascular complications is not clear. In the present study, we examined plasma total AM levels, and their association with different markers of endothelial dysfunction and with other established risk factors for cardiovascular diseases, in patients with Type 1 DM. We studied a total of 155 patients, 117 patients without any kind of vascular complications, 24 patients with retinopathy only, and 14 patients with retinopathy and microalbuminuria but normal renal function. None of them had clinical evidence of atherosclerotic disease. Compared with the control group (64 healthy participants), patients had raised fibrinogen, soluble E-selectin ((s)E-selectin), vascular cellular adhesion molecule (VCAM), angiotensin converting enzyme (ACE), and von Willebrand factor (vWf) (P<.001 in all cases), but plasma total AM, endothelin (ET), sialic acid, and homocysteine were not raised. In the diabetic group, AM levels correlated significantly with sialic acid (r=.16; P<.05), but a more significant correlation was found with fibrinogen (r=.30; P<.001). No correlation was found with the other parameters studied. In summary, plasma total AM levels seem to correlate with inflammatory markers but not with endothelial dysfunction markers in Type 1 diabetic patients without atherosclerotic disease.
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PMID:Levels of plasma total adrenomedullin are related with two acute phase inflammatory reactants (fibrinogen and sialic acid) but not with markers of endothelial dysfunction in Type 1 diabetes Adrenomedullin and vascular risk factors in Type 1 DM. 1586 60

Chronic inhibition of nitric oxide (NO) synthesis by administration of high dose of N(G)-nitro-L-arginine methylester (L-NAME) induces vascular inflammation and subsequent atherosclerosis. We aimed to investigate whether the methanol extract of Sorbus commixta cortex (MSC) is able to prevent inflammatory process in a rat model of L-NAME-induced atherosclerosis. Chronic treatment with low or high doses of MSC prevented the L-NAME-induced increase in monocyte chemoattractant protein-1 (MCP-1) and nuclear factor-kappaB (NF-kappaB) p65 expressions as well as adhesion molecules including intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1), and E-selectin in aorta. In addition, increased endothelin-1 (ET-1) and angiotensin converting enzyme (ACE) expressions and decreased endothelial cell NO synthase (ecNOS) expression in aorta from L-NAME treated group was reversed by treatment with MSC. From the histological examination, aortic segment from the L-NAME-treated rats revealed a thickening of intima and media, which was ameliorated by treatment with MSC. In conclusion, our results indicate that MSC can prevent atherosclerosis by inhibiting vascular over-expressions of vasoactive materials, pro-inflammatory transcription factor, and adhesion molecules and by augmenting ecNOS in chronic L-NAME-treated rat model.
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PMID:Effect of methanol extract of Sorbus cortex in a rat model of L-NAME-induced atherosclerosis. 1599 6

Placenta-derived chymotrypsin-like protease (CLP/chymase) promotes endothelial P-selectin and E-selectin expression, which may be responsible for the increased neutrophil/endothelial interactions in preeclampsia (PE). However, little is known about this protease expression and production in human placenta. This study was undertaken to determine the distribution and gene expression of CLP in human placenta. Human placental tissues were obtained immediately after delivery from normal and PE pregnancies. We examined (1) CLP/chymase immunoactivity by immunohistochemical staining of villous tissue sections; (2) trophoblast mRNA and protein expression for chymase by RT-PCR and Western blot analysis; (3) chymase cDNA sequencing in isolated trophoblast cells (TCs); and (4) release of CLP by placental villous tissue cultured under 2% and 20% O(2). We found (1) CLP expression is mainly localized in the epithelial layer of syncytiotrophoblasts; (2) both mRNA and protein expression are significantly (p<0.05) upregulated in TCs isolated from PE vs. normal placentas; (3) TC chymase cDNA sequence and the deduced amino acid sequence are 100% identical to that reported for the human heart; and (4) villous tissue releases more chymotrypsin when cultured with 2% O(2). We conclude that (1) the DNA and protein sequence for chymase in placental trophoblast cells are the same as those reported in the human heart; (2) CLP/chymase expression is upregulated in TCs during PE; and (3) lowered oxygen condition promotes CLP release by placental TCs. Since chymase is a potent non-ACE angiotensin II producing enzyme, our data suggest that if placenta-derived CLP/chymase is released into the maternal circulation, it may contribute to the cardiovascular complications associated with PE.
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PMID:Increased chymotrypsin-like protease (chymase) expression and activity in placentas from women with preeclampsia. 1669 79

Atherosclerosis is a chronic inflammatory process. The adhesion of leukocytes to the vascular endothelium, mediated by endothelial cell adhesion molecules including vascular adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), and E-selectin, is the pivotal early event in atherogenesis. Inflammatory cytokines could activate redox-sensitive transcription factors and induce endothelial expression of adhesion molecules, which could be inhibited to various degrees by different antioxidants suggesting the potential role of endogenous reactive oxygen species (ROS) in atherogenesis. Many clinical drugs that against cardiovascular diseases have exhibited antioxidant effects; these drugs simultaneously inhibit endothelial adhesion molecule expression, such as aspirin, probucol, HMG-CoA reductase inhibitors, angiotensin receptor blockers, angiotensin converting enzyme inhibitors, peroxisome proliferator-activated receptor alpha and gamma ligands, calcium channel blockers, beta-adrenergic blockers, etc. In addition, we have previously demonstrated that Ginkgo biloba extract, a Chinese herb with antioxidant activity, could significantly suppress inflammatory cytokine-stimulated endothelial adhesiveness to human monocytic cells by attenuating intracellular ROS formation, redox-senstive transcription factor activation, and VCAM-1 as well as ICAM-1 expression in human aortic endothelial cells. The similar anti-atherosclerosis effects have been also shown in other Chinese herbs or dietary supplements with antioxidant activity such as magnolol and salvianolic acid B either in vitro or in vivo. Thus, oxidative stress is critical to endothelial adhesiveness in atherogenesis. The inhibition of endothelial adhesion molecule expression by drugs/agents with antioxidant activity may serve as a potential therapeutic strategy for clinical atherosclerosis.
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PMID:Anti-inflammatory effects of different drugs/agents with antioxidant property on endothelial expression of adhesion molecules. 1737 73

This study attempts to confirm previous findings of altered serum soluble E-selectin and laminin in workers exposed to volatile organic chemicals VOCs and further explore evidence of endothelial cell disturbances in workers exposed to (VOCs) and mercury vapour. Serum angiotensin converting enzyme (ACE), soluble E-selectin and laminin were measured in a cross sectional study of workers exposed to a small range of VOCs (n = 21), mercury vapour (n = 32) and a control group (n = 50). Both endothelial markers, ACE and E-selectin were significantly higher in mercury- and VOC-exposed workers. Laminin was significantly lower than controls in the VOC exposed. These results confirm our previous initial findings in workers exposed to VOCs of endothelial disturbances and decreased serum levels of a constituent of basement membranes, namely laminin. In the mercury exposed workers who had relatively high occupational exposure for the UK, there was also evidence of endothelial disturbances. The ubiquitous nature of endothelial cells and the underlying structural basement membrane associated with the vasculature means that it is impossible to state with any certainty the site of the action of these chemicals. However due to the ease of absorption of VOCs and mercury via the pulmonary system, and the metabolism of VOCs in the lungs themselves, it is probable that the initial site of the disturbances noted is in lung endothelia and associated basement membrane.
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PMID:Serum angiotensin converting enzyme, soluble E-selectin and laminin in subjects occupationally-exposed to volatile organic chemicals and mercury vapour. 2389 82

This study investigates the effect of ACE2 activation on leptin-induced changes in systolic blood pressure (SBP), proteinuria, endothelial activation and ACE2 expression during pregnancy in Sprague-Dawley rats. Pregnant rats were given subcutaneous injection of either saline, or leptin, or leptin plus xanthenone (ACE2 activator), or xanthenone (XTN) alone. SBP, serum ACE, ACE2, endothelin-1, E-selectin and ICAM-1 levels were estimated; also their gene expressions were determined in the kidney and aorta respectively. Compared to control, SBP was higher in the leptin-only treated group (P<0.001) and lower in rats treated with xanthenone alone (P<0.01). Proteinuria, markers of endothelial activation were significantly higher than controls in leptin-only treated rats (P<0.05). ACE2 activity and expression were lower in leptin-only treated rats when compared to controls (P<0.05). It seems, leptin administration during pregnancy significantly increases SBP, proteinuria, endothelial activation, but decreases ACE2 level and expression. These effects are prevented by concurrent administration of xanthenone.
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PMID:ACE2 activation by xanthenone prevents leptin-induced increases in blood pressure and proteinuria during pregnancy in Sprague-Dawley rats. 2520 67


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