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)

Hepatocellular carcinoma (HCC) is one of the most important medical problems facing the Asian-Pacific region, where the prevalence of chronic hepatitis B and C is so high. Every year, we have approximately 500 admissions to our department due to this malignancy. It is of utmost importance that we have efficient screening, diagnosis and treatment. Over the past several years, there has been steady improvement in elucidating the super-high risk group for HCC, and in the management of these patients. I discuss how effectively we can screen patients by using three tests, conventional AFP, AFP-L3 (lectin fraction) and DCP (des-gamma-carboxy-prothrombin). With these tests we can detect HCC as small as 10 mm. In addition, imaging technology including CT-angiography can effectively pick up small cancer nodules. However, they are not always readily available in all Asian countries. Thus, diagnostic procedures and treatment methods can be modified in each country depending on the situation. One such treatment modality is the percutaneous therapy. The recent introduction of radiofrequency ablation (RFA) has dramatically changed our daily clinical practice. The time needed to treat cancer nodules of 2 to 3 cm in size has been reduced from 1 month or longer with ethanol injection to less than a week with RFA. However, the most important issue is to prevent infection and progression from chronic hepatitis to HCC. The recent introduction of improved antiviral therapy makes us feel optimistically that we might eventually have a comprehensive strategy for HCC in the region where it is most needed.
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PMID:Resolution of liver cirrhosis and prevention of hepatocellular carcinoma by interferon therapy against chronic hepatitis C. 1279 82

Lectins are known to bind to the intestinal brush border membrane and induce antinutritional effects such as disruption of the brush border membrane (BBM) and reduced nutrient digestibility in laboratory rodents. Because soybean lectin (SBL) is usually present in poult starter diets, 2 similar experiments with starting turkey poults were conducted to investigate the effects of purified SBL on growth performance and nutrient digestibility. Experimental diets were a corn starch-casein based control (lectin-free) semipurified diet (PD), semipurified diets containing 0.024 or 0.048% soybean lectin (PDL, PDH), and a corn-soybean meal diet (SBD). Experimental diets were fed from hatch to 14 d. Antibodies specific for soybean lectin were detected in the serum of poults fed the PDL and PDH diets, implying that the SBL in these diets remained active in the digestive tract. Poults fed the control PD or SBD grew equally well. The 0.024% SBL level in PDL had no significant detrimental effect on any parameters assessed in the 2 experiments. In contrast, the 0.048% SBL level in the PDH gave inconsistent results for feed efficiency (FE) and brush border enzyme levels. For instance, on d 6 in experiment 2, poults fed the PDH had poorer FE (P < 0.05) compared with the control PD treatment, but had similar FE to poults fed the PD in experiment 1. In conclusion, SBL present at levels up to 0.024% of the diet would not cause antinutritional effect in turkey poults up to 2 wk of age.
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PMID:Response of turkey poults to soybean lectin levels typically encountered in commercial diets. 1. Effect on growth and nutrient digestibility. 1538 8

Lectins are capable of altering intestinal morphology by binding to and disrupting the intestinal brush border membrane. They are also known to alter the weight of lymphoid organs. Therefore, we evaluated the effect of soybean lectin (SBL) on intestinal morphology and lymphoid organ weights of poults fed diets containing SBL. Dietary treatments evaluated in this study included a cornstarch and casein-based control (lectin-free) semipurified diet (PD) and semipurified diets containing 0.024 or 0.048% SBL (PDL and PDH, respectively). Experimental diets were fed from hatch to 14 d. Morphological evaluation of the intestine involved measurement of the villi height and perimeter, crypt depth, villus:crypt, and thickness of the muscle layer in the jejunum. Intestinal physical characteristics were also determined by measuring intestinal weight, length, and volume. Results indicated that 0.048% SBL in PDH increased villus:crypt and reduced total intestinal length in turkey poults. In addition, both the 0.024 and 0.048% dietary SBL levels reduced thymus weights. It was concluded that dietary SBL up to 0.048% enhanced intestinal development by increasing villus:crypt, but might alter the structural integrity of lymphoid organs.
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PMID:Response of turkey poults to soybean lectin levels typically encountered in commercial diets. 2. Effect on intestinal development and lymphoid organs. 1667 65

Human serum amyloid P component (SAP) is a glycoprotein circulating in the blood and found in association with all types of amyloid (malfolded potein aggregates) examined so far. Despite uncertainties regarding the precise function of SAP in vivo, the lectin-like properties of this Ca(2+)-activated protein with affinity for anionic saccharides and malfolded proteins are well known. The propensity to form homomeric penta- or decamers in solution and the selfaggregation in the presence of Ca(2+) as well as the tendency of SAP to attach to uncoated fused silica have precluded the analysis of SAP by microelectrophoretic methods. We now work out conditions to characterize the binding of Ca(2+) and Mg(2+) and the binding of heparin to SAP in the presence of divalent metal ions by ACE. The results show a strong binding of heparin (sub-muM apparent dissociation constants) even in the abscence of Ca(2+) at low ionic strength, pH 8.2. Also, a selective interaction with Ca(2+) compared with Mg(2+) is demonstrated. The approach will further the use of microelectrophoretic methods to examine the interactions of SAP with ligands of putative pathophysiological relevance such as lipopolysaccharides and misfolded proteins.
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PMID:Binding of Ca2+, Mg2+, and heparin by human serum amyloid P component in affinity capillary electrophoresis. 1681 62

This review article is aimed at assessing the recent progress made in affinity nano-LC and affinity CEC performed in capillaries and microchips. A variety of biospecific interactions is covered including lectin affinity, immunoaffinity, immobilized metal affinity, sugar-based affinity, protein A affinity, protein G affinity, aptamer affinity, enzyme affinity, and other miscellanea. ACE involving affinity interaction in free solution is not covered in this review article. Also, affinity-based separations involving chiral recognition are not the subject of this review article because they are the topic of a more specialized review article on chiral separations in this special issue. A total of 31 papers published in the period 1998-2006 have been discussed in this review article.
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PMID:Biospecific interaction (affinity) CEC and affinity nano-LC. 1717 49

Although it is well known that the hepatocellular carcinoma (HCC) is an ominous complication in patients with liver cirrhosis, there has been no approved drug to prevent the development of HCC to date. We previously reported that the combined treatment of vitamin K2 (VK) and angiotensin-converting enzyme inhibitor (ACE-I) significantly suppressed the experimental hepatocarcinogenesis. A 66-year-old Japanese woman with hepatitis C virus (HCV)-related liver cirrhosis developed a dysplastic nodule in the liver detected by enhanced computed tomography along with elevation of the tumor markers, namely, alpha-fetoprotein (AFP) and lectin-reactive demarcation (AFP-L3), suggesting the presence of latent HCC. After oral administration of VK and ACE-I, the serum levels of both AFP and AFP-L3 gradually decreased without any marked alteration of the serum aminotransferase activity. After one-year treatment, not only the serum levels of AFP and AFP-L3 returned to the normal ranges, but also the dysplastic nodule disappeared. Since both VK and ACE-I are widely used without serious side effects, this combined regimen may become a new strategy for chemoprevention against HCC.
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PMID:Combined treatment of vitamin K2 and angiotensin-converting enzyme inhibitor ameliorates hepatic dysplastic nodule in a patient with liver cirrhosis. 1758 9

Increased levels of low-density lipoproteins are well-established risk factors of endothelial dysfunction and the metabolic syndrome. In this study, we evaluated the effect of native low-density lipoprotein (nLDL) and oxidized LDL (oxLDL) on the expression of genes of the renin-angiotensin system (angiotensin-converting enzyme, ACE; angiotensin II type 1 receptor, AT(1)) and their receptors (low-density lipoprotein receptor: LDLR; lectin-like oxLDL receptor: LOX-1; toll-like receptor 4: TLR4) in primary cultures of human umbilical vein endothelial cells. ACE and AT(1) expressions were significantly increased after stimulation with nLDL and oxLDL. OxLDL receptor LOX-1 showed a maximum induction after 7 hours. Increased LOX-1 protein expression in response to oxLDL could be blocked by a LOX-1-specific antibody. TLR4 expression was increased by nLDL and oxLDL as well. We conclude that LDL and oxLDL can activate the renin-angiotensin system and their receptors LDLR, LOX-1, and TLR4 in human endothelial cells. These data suggest a novel link between hypercholesterolemia and hypertension in patients with the metabolic syndrome.
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PMID:Low-density lipoproteins induce the renin-angiotensin system and their receptors in human endothelial cells. 1799 34

We analyzed the effect of hypertension on postischemic vasculogenesis. Ischemia was induced by right femoral artery ligature in Wistar Kyoto rats (WKY) or spontaneously hypertensive rats (SHR) treated with or without angiotensin-converting enzyme inhibitor (Perindopril, 0.76 mg/kg/d) and angiotensin type 1 receptor blocker (losartan, 30 mg/kg/d). Basal postischemic neovascularization was reduced in SHR compared to WKY (P<0.05, n=8). Treatment with ACE inhibitor or angiotensin type 1 receptor blocker decreased blood pressure levels by 1.4- and 1.3-fold (P<0.001), respectively and restored vessel growth in SHR to WKY levels. Interestingly, 14 days after bone-marrow mononuclear cell (BM-MNC) transfusion, angiographic scores, capillary density, and foot perfusion were decreased by 1.4-, 1.5-, and 1.2-fold, respectively in SHR transfused with BM-MNCs isolated from SHR compared to those receiving BM-MNCs of WKY (P<0.05, n=6). Alteration in BM-MNCs proangiogenic potential was likely related to the reduction in their ability to mobilize into peripheral circulation, as revealed by the 2.9-fold decrease in number of circulating CD34+/CD117+ cells (P<0.001) and to differentiate into cells with endothelial phenotype, as revealed by the 2.1-fold reduction in percentages of DilLDL/BS-1 lectin positive cells (P<0.001). In addition, reactive oxygen species (ROS) levels were increased by 2.2-fold in SHR BM-MNCs compared to WKY BM-MNCs (P<0.01), as assessed by L-012 luminescence. Cotreatment with ACE inhibitor, angiotensin type 1 receptor blocker, or antioxidants (NAC 3 mmol/L, Apocynin 200 micromol/L) reduced ROS levels, improved the number of DilLDL/BS-1 lectin-positive cells by around 1.5-fold, and restored BM-MNCs proangiogenic effects in ischemic hindlimb. In conclusion, alteration in progenitor cell proangiogenic function may participate to the hypertension-induced impairment in postischemic revascularization.
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PMID:Hypertension impairs postnatal vasculogenesis: role of antihypertensive agents. 1842 93

Angiotensin-converting enzyme 2 (ACE2) is a newly discovered homolog of ACE whose actions oppose those of angiotensin II (AngII). However, the underlying mechanisms by which ACE2 effectively suppresses early atherosclerotic lesions remain poorly understood. Here, we show, both in vitro and in vivo, that ACE2 inhibited the development of early atherosclerotic lesions by suppressing the growth of vascular smooth muscle cells (VSMCs) and improving endothelial function. In a relatively large cohort animal study (66 rabbits), aortic segments transfected by Ad-ACE2 showed significantly attenuated fatty streak formation, neointimal macrophage infiltration, and alleviation of impaired endothelial function. Segments also showed decreased expression of monocyte chemoattractant protein 1, lectin-like oxidized low-density lipoprotein receptor 1, and proliferating cell nuclear antigen, which led to the delayed onset of atherosclerotic lesions. At the cellular level, ACE2 significantly modulated AngII-induced growth and migration in human umbilical vein endothelial cells and VSMCs. The antiatherosclerotic effect of ACE2 involved down-regulation of the ERK-p38, JAK-STAT, and AngII-ROS-NF-kappaB signaling pathways and up-regulation of the PI3K-Akt pathway. These findings revealed the molecular mechanisms of the antiatherosclerotic activity of ACE2 and suggested that modulation of ACE2 could offer a therapeutic option for treating atherosclerosis.
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PMID:Angiotensin-converting enzyme 2 attenuates atherosclerotic lesions by targeting vascular cells. 2079 44

Successful procedures for the isolation and culture of large-vessel endothelial cells (EC), were first reported in the early seventies (1,2). Since then, microvascular EC have been isolated from various organs, such as adrenal gland (3), brain (4), skin (5), retina (6), and myocardium (7). The initial steps of the conventional methods for EC isolation involve mechanical and/or enzymatic dissociation of the tissues, followed by filtration and pelleting of cells. A number of special techniques have been developed to eliminate contaminating cell types and enrich endothelial cells in mixed cell populations. These include: manual removal of nonendothelial cell types; use of selective media; plating cells on gelatin or fibronectin-coated dishes, and Percoll gradient centrifugation (8,9). The main problem with the conventional methods is that they are labor intensive and often do not produce pure EC populations. A more advanced approach is to use fluorescent-activated cell sorting (FACS) which allows sorting based on specific surface antigens or metabolic differences. Auerbach et al. used FACS for EC isolation, using an antibody against angiotensin converting enzyme (10). Later, Voyta et al. sorted EC, based on their uptake of acetylated low-density lipoprotein (11). Cell separation techniques using magnetic affinity are based on similar principles as the FACS, but do not involve expensive equipment. In this chapter, we describe liver endothelial cell isolation, using lectin-coated magnetic beads (12).
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PMID:Lectins as tools for the purification of liver endothelial cells. 2137 72


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