Cholesterol Journal Articles

Record 5841 to 5860

Enhancement of migration activity in cholesterol-poor endothelial cells by pre-treating with HMG-CoA reductase inhibitors
Ma, L., I. Morita, et al. (1994), Biochem Biophys Res Commun 203(2): 1355-61.
Abstract: When bovine endothelial cells isolated from carotid arteries were cultured with a low density lipoprotein(LDL)-deficient serum for 2 days, their intracellular free cholesterol levels decreased. Under this condition, exposure of the endothelial cells to simvastatin and pravastatin, HMG-CoA reductase inhibitors used clinically, resulted in further decrease in the free cholesterol levels. The migration activity was enhanced in the cells cultured with the LDL-deficient serum and it was more enhanced in the cells treated with HMG-CoA reductase inhibitors under the LDL-deficient serum condition. These results suggest that cholesterol plays a negative role in wound healing in arterial walls and acts as one of the risk factors for arteriosclerosis.

Enhancement of scavenger receptor class B type I-mediated selective cholesteryl ester uptake from apoA-I(-/-) high density lipoprotein (HDL) by apolipoprotein A-I requires HDL reorganization by lecithin cholesterol acyltransferase
Temel, R. E., J. S. Parks, et al. (2003), J Biol Chem 278(7): 4792-9.
Abstract: The severe depletion of cholesteryl ester (CE) in adrenocortical cells of apoA-I(-/-) mice suggests that apolipoprotein (apo) A-I plays an important role in the high density lipoprotein (HDL) CE selective uptake process mediated by scavenger receptor BI (SR-BI) in vivo. A recent study showed that apoA-I(-/-) HDL binds to SR-BI with the same affinity as apoA-I(+/+) HDL, but apoA-I(-/-) HDL has a decreased V(max) for CE transfer from the HDL particle to adrenal cells. The present study was designed to determine the basis for the reduced selective uptake of CE from apoA-I(-/-) HDL. Variations in apoA-I(-/-) HDL particle diameter, free cholesterol or phospholipid content, or the apoE or apoA-II content of apoA-I(-/-) HDL had little effect on HDL CE selective uptake into Y1-BS1 adrenal cells. Lecithin cholesterol acyltransferase treatment alone or addition of apoA-I to apoA-I(-/-) HDL alone also had little effect. However, addition of apoA-I to apoA-I(-/-) HDL in the presence of lecithin cholesterol acyltransferase reorganized the large heterogeneous apoA-I(-/-) HDL to a more discrete particle with enhanced CE selective uptake activity. These results show a unique role for apoA-I in HDL CE selective uptake that is distinct from its role as a ligand for HDL binding to SR-BI. These data suggest that the conformation of apoA-I at the HDL surface is important for the efficient transfer of CE to the cell.

Enhancement of the antigen-presenting function of monocytes by cholesterol: possible relevance to inflammatory mechanisms in extrinsic allergic alveolitis and atherosclerosis
Hughes, D. A., P. J. Townsend, et al. (1992), Clin Exp Immunol 87(2): 279-86.
Abstract: Extrinsic allergic alveolitis (EAA) (synonym: hypersensitivity pneumonitis) is a hypersensitivity lung disease characterized by lymphocytic infiltrates in the pulmonary interstitial tissues. We have previously reported that the numbers of lymphocytes in bronchoalveolar lavage (BAL) samples in this disease correlate with levels of cholesterol and neutral lipid-laden 'foamy' macrophages. We have also reported that the macrophages express an increased density of MHC class II antigens (in particular HLA-DQ) which are known to be essential for antigen recognition by T lymphocytes. The aim of the present study was to explore whether cholesterol is capable of enhancing the antigen-presenting function of mononuclear phagocytes by modulating the expression of HLA-D region products. Incubation of purified monocytes from healthy volunteers with cholesterol in serum-free medium induced a significant increase in both the percentages of monocytes expressing HLA-DQ (P less than 0.02) and in the intensity of expression of the three HLA-D sub-region products, HLA-DQ, -DP and -DR (P less than 0.02, less than 0.01, less than 0.05, respectively). The cholesterol pre-incubated monocytes also exhibited enhanced antigen-presenting function (P less than 0.05), compared with controls pre-incubated without cholesterol. These findings indicate that increases in cholesterol in the extracellular milieu may augment antigen presentation by modulating the expression of HLA-D region products on antigen-presenting cells. Apart from EAA, this observation may also have relevance to inflammatory mechanisms in atherosclerosis, where 'foamy' macrophages also occur in association with hypercholesterolaemia.

Enhancement of thrombotic arterial occlusion following cholesterol feeding in the guinea-pig: a role for thromboxane A2
Hirata, Y., K. Umemura, et al. (1994), Prostaglandins Leukot Essent Fatty Acids 51(2): 81-6.
Abstract: We have developed a photochemical model to induce thrombotic occlusion of the guinea-pig femoral artery. Using this model, we investigated the effect of cholesterol feeding on arterial occlusion time in the guinea-pig. Animals were divided into two groups, one on standard diet and the other on standard diet containing 0.5% cholesterol for 3 weeks. The time for femoral artery occlusion was significantly shorter (p < 0.05) in cholesterol fed animals as compared to the control group. In vitro collagen-, U-46619- (a thromboxane A2 adenosine diphosphate analogue) and (ADP)-induced platelet aggregation responses in whole blood in cholesterol-fed animals were increased 13-, 10- and 4-fold, respectively. U-46619- and collagen-induced washed platelet aggregation responses were also significantly enhanced by cholesterol feeding (p < 0.01). Further, TXA2 generation by collagen-stimulated washed platelets in cholesterol-fed animals increased similar to the platelet aggregation responses. However, platelet-activating factor (PAF)-induced platelet aggregation in whole blood was relatively unaffected by cholesterol feeding. 11-dehydro TXB2 levels in plasma were increased significantly by cholesterol feeding. Our observations suggest that increased plasma TXA2 level and platelet aggregation response to TXA2 and stimulated TXA2 synthesis in platelets play a role in enhanced arterial occlusion in cholesterol fed guinea-pigs.

Enhancing adherence to referral advice given at blood cholesterol screenings: impact on participant follow-up and physician behavior
Lefebvre, R. C., S. W. Banspach, et al. (1991), Health Educ Res 6(4): 405-13.
Abstract: Adherence to referral recommendations given to participants at blood cholesterol screening programs is a critical aspect of these efforts to help detect and control high blood cholesterol in the US adult population. In this study, 386 participants who had received two consecutive blood cholesterol measurements above 240 mg/dl (6.21 mmol/l) were interviewed by telephone 3 months after their second measurement (May 1987 - May 1988). Approximately 40% of respondents had seen a physician by the time of the interview; another 30% reported having scheduled an appointment. There was no significant difference in adherence behavior between participants who received a letter reiterating the referral and those who did not. However, participants who received the letter reported greater physician attention to the evaluation and treatment of their high blood cholesterol, primarily because these participants stated that they visited their physician for their high blood cholesterol. Significantly higher rates of further blood tests, cholesterol education material distribution, cholesterol-lowering medication prescription and patient-physician discussions about cholesterol were the result. These findings suggest that consumers can be effective in stimulating and reinforcing physician practice behaviors related to cholesterol control. However, strategies must be crafted so that consumers are aware of, and appreciate, the necessity of seeking physician care when they become aware of a high blood cholesterol level.

Enhancing effect of dietary cholesterol and inhibitory effect of pravastatin on allergic pulmonary inflammation
Yeh, Y. F. and S. L. Huang (2004), J Biomed Sci 11(5): 599-606.
Abstract: To elucidate the link between the intake of animal fat and asthma, a murine model was developed to examine the effect of dietary cholesterol on pulmonary allergic inflammation. Male C57BL6 mice were fed either a control diet or a diet supplemented with 2% cholesterol. Following sensitization and inhalation exposure to ovalbumin, the bronchoalveolar lavage fluid of mice in the cholesterol group contained higher numbers of eosinophils and elevated levels of IL-5, PGE(2), and MCP-1. In addition, dietary cholesterol also resulted in elevated production of IL-4 and IFN-gamma by lymphocytes isolated from the lungs. These inflammatory indicators were all significantly correlated with serum cholesterol levels. In contrast to the effect of dietary cholesterol, adding pravastatin to the drinking water significantly reduced eosinophil infiltration and the levels of IL-5, PGE(2) and MCP-1 in lavage fluid. Although dietary cholesterol did not alter baseline IL-12 in the lungs, in mice challenged with ovalbumin the IL-12 levels were reduced in the cholesterol group and elevated significantly in the pravastatin group. The results suggest that dietary cholesterol might enhance pulmonary allergic inflammation, possibly involving both nonspecific inflammatory processes and lymphocyte activities.

Enhancing reverse cholesterol transport: the case for phosphatidylcholine therapy
Pownall, H. J. and C. Ehnholm (2005), Curr Opin Lipidol 16(3): 265-8.

Enprostil impairs cholesterol and fat absorption
Vanhanen, H. and T. A. Miettinen (1995), Scand J Gastroenterol 30(1): 33-7.
Abstract: BACKGROUND: Enprostil, a synthetic dehydroprostaglandin E2 structural analogue primarily developed for treatment of gastritis, has been shown also to lower serum cholesterol. METHODS: We studied cholesterol metabolism in seven hypercholesterolemic subjects before, during, and after a low-dose enprostil (18 micrograms/day) treatment, measuring serum lipids, cholesterol absorption by an oral double-isotope method, fecal cholesterol elimination by the balance technique, and fecal fat. In addition, an oral fat load test with vitamin A was performed. RESULTS: The drug treatment reduced serum concentrations of total and low-density lipoprotein (LDL) cholesterol by 8.2% and 7.9% (p < 0.05), respectively, and cholesterol absorption efficiency by 18% (p < 0.05), and increased fecal output of neutral sterols by 20% (p < 0.05), bile acids by 24% (NS), and cholesterol synthesis by 30% (p < 0.05). Postabsorptive concentrations of triglycerides and vitamin A in chylomicrons were reduced 3-4 h after the intake of the test meal. Fecal fat excretion was doubled during the enprostil treatment. CONCLUSIONS: Enprostil reduces serum cholesterol concentrations, apparently by inhibiting cholesterol absorption so that fecal cholesterol elimination is increased in association with a mild fat malabsorption. Enhanced intestinal motility may contribute to these changes, frequently causing abdominal fullness or mild pain without diarrhea.

Enrichment of canalicular membrane with cholesterol and sphingomyelin prevents bile salt-induced hepatic damage
Amigo, L., H. Mendoza, et al. (1999), J Lipid Res 40(3): 533-42.
Abstract: These studies were undertaken to characterize the role of plasma membrane cholesterol in canalicular secretory functions and hepatocyte integrity against intravenous taurocholate administration. Cholesterol and sphingomyelin concentrations and cholesterol/phospholipid ratios were significantly increased in canalicular membranes of diosgenin-fed rats, suggesting a more resistant structure against solubilization by taurocholate. During taurocholate infusion, control rats had significantly decreased bile flow, whereas diosgenin-fed animals maintained bile flow. Maximal cholesterol output increased by 176% in diosgenin-fed rats, suggesting an increased precursor pool of biliary cholesterol in these animals. Maximal phospholipid output only increased by 43% in diosgenin-fed rats, whereas bile salt output remained at control levels. The kinetics of glutamic oxalacetic transaminase, lactic dehydrogenase, and alkaline phosphatase activities in bile showed a significantly faster release in control than in diosgenin-fed rats. After 30 min of intravenous taurocholate infusion, necrotic hepatocytes were significantly increased in control animals. Preservation of bile secretory functions and hepatocellular cytoprotection by diosgenin against the intravenous infusion of toxic doses of taurocholate was associated with an increased concentration of cholesterol and sphingomyelin in the canalicular membrane. The increase of biliary cholesterol output induced by diosgenin was correlated to the enhanced concentration of cholesterol in the canalicular membrane.

Enrichment of endoplasmic reticulum with cholesterol inhibits sarcoplasmic-endoplasmic reticulum calcium ATPase-2b activity in parallel with increased order of membrane lipids: implications for depletion of endoplasmic reticulum calcium stores and apoptosis in cholesterol-loaded macrophages
Li, Y., M. Ge, et al. (2004), J Biol Chem 279(35): 37030-9.
Abstract: Macrophages in advanced atherosclerotic lesions accumulate large amounts of unesterified, or "free," cholesterol (FC). FC accumulation induces macrophage apoptosis, which likely contributes to plaque destabilization. Apoptosis is triggered by the enrichment of the endoplasmic reticulum (ER) with FC, resulting in depletion of ER calcium stores, and induction of the unfolded protein response. To explain the mechanism of ER calcium depletion, we hypothesized that FC enrichment of the normally cholesterol-poor ER membrane inhibits the macrophage ER calcium pump, sarcoplasmic-endoplasmic reticulum calcium ATPase-2b (SERCA2b). FC enrichment of ER membranes to a level similar to that occurring in vivo inhibited both the ATPase activity and calcium sequestration function of SERCA2b. Enrichment of ER with ent-cholesterol or 14:0-18:0 phosphatidylcholine, which possess the membrane-ordering properties of cholesterol, also inhibited SERCA2b. Moreover, at various levels of FC enrichment of ER membranes, there was a very close correlation between increasing membrane lipid order, as monitored by 16-doxyl-phosphatidycholine electron spin resonance, and SERCA2b inhibition. In view of these data, we speculate that SERCA2b, a conformationally active protein with 11 membrane-spanning regions, loses function due to decreased conformational freedom in FC-ordered membranes. This biophysical model may underlie the critical connection between excess cholesterol, unfolded protein response induction, macrophage death, and plaque destabilization in advanced atherosclerosis.

Entamoeba histolytica is unable to use free cholesterol, phospholipids, and fatty acids under axenic cultivation conditions
Mata-Cardenas, B. D., J. Vargas-Villarreal, et al. (2000), Arch Med Res 31(4 Suppl): S212-3.

Enterostatin (VPDPR) and its peptide fragment DPR reduce serum cholesterol levels after oral administration in mice
Takenaka, Y., F. Nakamura, et al. (2003), Biosci Biotechnol Biochem 67(7): 1620-2.
Abstract: We found that enterostatin (VPDPR), an anorexigenic peptide for a high-fat diet, significantly reduces serum cholesterol levels after oral administration of 100 mg/kg for 3 days in mice fed a high cholesterol-cholic acid diet. DPR, a peptide fragment of VPDPR, also had hypocholesterolemic activity at a dose of 50 mg/kg. Food intake was not suppressed under these dietary conditions. Fecal excretion of cholesterol and bile acids was increased significantly by both VPDPR and DPR. Interestingly, DPR induced hypocholesterolemic effects just two hours after a single oral administration at a dose of 100 mg/kg.

Entry of the lymphogranuloma venereum strain of Chlamydia trachomatis into host cells involves cholesterol-rich membrane domains
Jutras, I., L. Abrami, et al. (2003), Infect Immun 71(1): 260-6.
Abstract: Chlamydiae are bacterial pathogens which develop strictly inside the epithelial cells of their hosts. The mechanism used by chlamydiae to enter cells is not well characterized; however, it is thought to consist of a receptor-mediated process. In addition, the formation of clathrin-coated pits appears to be dispensable for chlamydiae to be internalized by host cells. Clathrin-independent endocytosis has recently been shown to occur through cholesterol-rich lipid microdomains, which are characterized by detergent insolubility. In the present study, we investigated whether these lipid domains play a role in Chlamydia trachomatis serovar L2 internalization by host cells. Our results show that after binding to HeLa cells, chlamydiae are associated with detergent-resistant lipid microdomains (DRMs), which can be isolated by fractionation of infected HeLa cells and flotation on a sucrose gradient. After internalization by HeLa cells, chlamydiae were still found in DRMs. In addition, extraction of plasma membrane cholesterol inhibited infection of HeLa cells by C. trachomatis. Many of the proteins associated with DRMs are glycosylphosphatidylinositol (GPI)-anchored proteins; however, our results could not identify a role for GPI-anchored proteins in the entry process. The same results were obtained for Chlamydia psittaci strain GPIC. We propose that cholesterol-rich domains participate in the entry of chlamydiae into host cells. Chlamydia binding to cholesterol-rich domains may lead to coalescence of the bacterial cells, which could trigger internalization by host cells.

Environmental estrogens: effects on cholesterol lowering and bone in the ovariectomized rat
Dodge, J. A., A. L. Glasebrook, et al. (1996), J Steroid Biochem Mol Biol 59(2): 155-61.
Abstract: Representative non-steroidal estrogens, from common environmental sources such as plants, pesticides, surfactants, plastics, and animal health products, demonstrated an ability to lower serum cholesterol and prevent bone loss. Specifically, select environmental estrogens (coumestrol, genistein, methoxychlor, bisphenol A, and zeranol) effectively lowered total serum cholesterol in an estrogen-dependent animal model, the ovariectomized rat. Of these entities, coumestrol, methoxychlor, and zeranol prevented ovariectomy-induced bone loss. In an in vitro environment, these compounds competed with 17beta-estradiol for estrogen receptor binding and stimulated cell proliferation in a human breast cancer cell line (MCF-7). In addition to their well-documented effects on reproductive tissue, various environmental estrogens can dramatically affect non-reproductive parameters such as cholesterol lowering and bone metabolism.

Enzymatic coupling of cholesterol intermediates to a mating pheromone precursor and to the ras protein
Schafer, W. R., C. E. Trueblood, et al. (1990), Science 249(4973): 1133-9.
Abstract: The post-translational processing of the yeast a-mating pheromone precursor, Ras proteins, nuclear lamins, and some subunits of trimeric G proteins requires a set of complex modifications at their carboxyl termini. This processing includes three steps: prenylation of a cysteine residue, proteolytic processing, and carboxymethylation. In the yeast Saccharomyces cerevisiae, the product of the DPR1-RAM1 gene participates in this type of processing. Through the use of an in vitro assay with peptide substrates modeled after a presumptive a-mating pheromone precursor, it was discovered that mutations in DPR1-RAM1 cause a defect in the prenylation reaction. It was further shown that DPR1-RAM1 encodes an essential and limiting component of a protein prenyltransferase. These studies also implied a fixed order of the three processing steps shared by prenylated proteins: prenylation, proteolysis, then carboxymethylation. Because the yeast protein prenyltransferase could also prenylate human H-ras p21 precursor, the human DPR1-RAM1 analogue may be a useful target for anticancer chemotherapy.

Enzymatic determination of cholesterol in bile without interference of bilirubin
Portugal, H., A. M. Pauli, et al. (1993), Ann Biol Clin (Paris) 51(2): 119-24.
Abstract: The authors describe an enzymatic method for cholesterol determination in bile after elimination of bilirubin interference. During sample pretreatment, bilirubin is oxidized by hydrogen peroxide produced by adding glucose, glucose oxidase and peroxidase. Excess hydrogen peroxide is oxidatively coupled with 4-amino-antipyrine and a phenolic derivative (P-hydroxybenzoic acid). Cholesterol is then measured by use of a CHOD-PAP kinetic fixed-time method adapted to two different centrifugal analyzers (Multistat and Monarch IL). This method has a good within-run precision (CV = 1.6%) and good linearity (up to 23 mmol/l). Results have been compared to gas-liquid chromatographic (method selected by the Lipids-Lipoproteins Commission of the SFBC). The allometric regression line is: y = 1.016 x - 0.07 with r = 0.9975 (P < 0.001).

Enzymatic determination of serum total and esterified cholesterol with the same reagents
Matsushita, M., T. Irino, et al. (1990), Clin Chim Acta 191(1-2): 97-9.

Enzymatic determination of triglyceride, free cholesterol, and total cholesterol in tissue lipid extracts
Carr, T. P., C. J. Andresen, et al. (1993), Clin Biochem 26(1): 39-42.
Abstract: Triglyceride, free cholesterol, and total cholesterol were quantified in lipid extracts of liver and thoracic aorta from nonhuman primates using commercially available enzymatic reagents. Lipids were solubilized in water by the addition of Triton X-100. Results of the enzymatic assays compared favorably with chemical assays of lipids separated by thin-layer chromatography. In addition to saving time, the present method has the advantage of measuring each lipid class from a single sample preparation. Furthermore, the procedure has been adapted for use with microtiter plates that conserve both sample and reagent.

Enzymatic methods for quantitative determination of total cholesterol in blood serum
Pedchenko, V. V. and V. N. Malakhov (1991), Vopr Med Khim 37(4): 85-91.
Abstract: Advantages and disadvantages of enzymatic assays of total cholesterol content in human blood serum are reviewed. Factors, affecting these assays are discussed: specificity of the enzymes used (cholesterol esterase and cholesterol oxidase), conditions of analysis and composition of the reaction mixture, interference with components of blood serum. Adaptation of the enzymatic assays of total cholesterol estimation for various types of biochemical analyzers, including systems containing immobilized enzymes, is considered.

Enzymatic properties of polyethylene glycol-modified cholesterol esterase in organic solvents
Mori, S., Y. Nakata, et al. (1992), Biotechnol Appl Biochem 16(1): 101-5.
Abstract: The solvent dependency and substrate specificity of polyethylene glycol (PEG)-modified cholesterol esterase (CEH) catalyzing cholesterol ester synthesis in organic solvents were studied. When cholesterol and linoleic acid were used as the substrates, PEG-modified CEH synthesized cholesterol linoleate only in water-immiscible organic solvents. Among some solvents capable of solubilizing all of the reaction components (PEG-modified CEH, cholesterol, and linoleic acid), chloroform was most suitable for enzymatic cholesterol linoleate synthesis, and the synthetic activity for cholesterol linoleate decreased in the order chloroform, benzene, toluene, and cyclohexane. PEG-modified CEH synthesized various cholesterol esters with significant substrate specificity. The substrate specificity for cholesterol ester synthesis in benzene was analogous to that for cholesterol ester hydrolysis in aqueous solution.

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