| For medical practitioners and the general public - Cholesterol Journal Article Catalog. |
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| Vesicular and pronuclear glycoproteins in the pathogenesis of cholesterol lithiasis Jirsa, M., Jr., F. Smid, et al. (1998), Cas Lek Cesk 137(2): 48-51. Abstract: BACKGROUND: Several biliary proteins have been known to accelerate fusion of cholesterol rich phospholipid vesicles. Some of them are present in vesicular membrane, localisation of other proteins is unknown. Biliary glycoprotein has not been studied in consequence with pathogenesis of cholesterol lithiasis. METHODS AND RESULTS: Low molecular extravesicular proteins were separated from vesicles by gel filtration on a 1200mm column of Sephacryl S-300 HR. Immunoglobulins IgM, IgA, haptoglobin, biliary glycoprotein I (BGP I) and nonspecific crossreactive antigen were eluted along with vesicles. Albumin and alpha 1-acid glycoprotein were eluted later and must be extravesicular. CONCLUSIONS: Fact that BGP I (85 kDa membrane glycoprotein) eluted along with vesicles and not in albumin fraction suggests that it might be bound in vesicular membrane. As a known adhesion molecule it could thus play an important role in pathogenesis of cholesterol cholelithiasis. |
| Viability of Lactobacillus gasseri and its cholesterol-binding and antimutagenic activities during subsequent refrigerated storage in nonfermented milk Usman and A. Hosono (1999), J Dairy Sci 82(12): 2536-42. Abstract: The effect storage at 4 degrees C on the viability of Lactobacillus gasseri and its sodium taurocholate-deconjugating and cholesterol-binding abilities as well as desmutagenic activity was investigated. Unfermented milks containing L. gasseri strains SBT0274 and SBT0270 at 10(9) cfu/ml were prepared using 10% skim milk. Total and bile-tolerant lactobacilli for strains SBT0274 and SBT0270 generally decreased after 14 d of storage at 4 degrees C; however, viable cells of these strains were still at 10(8) cfu/ml after 28 d of storage. The amounts of cholic acid released and of cholesterol bound by strains SBT0274 and SBT0270 declined over time, especially at 21 d of storage. Antimutagenic activity of unfermented milk made from both strains was attributed to the bacterial cells, and the activity was stable during storage at 4 degrees C for 28 d. |
| Viewpoint on the Report of the National Cholesterol Education Program Expert Panel on Detection, Evaluation and Treatment of High Blood Cholesterol in Adults Kummerow, F. A. (1993), J Am Coll Nutr 12(1): 2-13. |
| Vimentin-dependent utilization of LDL-cholesterol in human adrenal tumor cells is not associated with the level of expression of apoE, sterol carrier protein-2, or caveolin Holwell, T. A., S. C. Schweitzer, et al. (1999), J Lipid Res 40(8): 1440-52. Abstract: SW-13 adrenal tumor cells that lack detectable intermediate filaments (IF-free) exhibit an impaired capacity to esterify lipoprotein-derived cholesterol compared with cells that contain vimentin filaments. IF-free cells were found to synthesize and secrete significant amounts of apoE, while apoE secretion was nearly undetectable in cell lines that spontaneously express vimentin. However, stable transfectants that express a mouse vimentin cDNA exhibited elevated levels of cholesterol esterification and apoE secretion compared with untransfected IF-free cells, indicating that apoE secretion is not directly related to the capacity of these cells to esterify cholesterol. Some of the cell lines that differed in the level of apoE synthesis and secretion had similar levels of apoE mRNA, suggesting that the differences in expression involve a post-transcriptional mechanism. Treatment of these cells with forskolin and IBMX, 8br-cAMP, or TPA had no effect on apoE secretion. The level of sterol carrier protein-2 (SCP(2)) synthesis and the distribution of SCP(2) between membrane and soluble cellular fractions was not observably different in cells that contained or lacked vimentin. SW-13 cell lines contained little or no detectable caveolin-1 or caveolin-2. These studies demonstrate that the difference in the capacity of these adrenal tumor cells that contain or lack vimentin filaments to esterify low density lipoprotein-cholesterol is not obviously associated with the level of expression or distribution of apoE, SCP(2), or caveolins. |
| Violent death and cholesterol reduction Samuel, P. (1992), Lancet 340(8810): 50-1. |
| VIP21/caveolin is a cholesterol-binding protein Murata, M., J. Peranen, et al. (1995), Proc Natl Acad Sci U S A 92(22): 10339-43. Abstract: VIP21/caveolin is localized to both caveolae and apical transport vesicles and presumably cycles between the cell surface and the Golgi complex. We have studied the lipid interactions of this protein by reconstituting Escherichia coli-expressed VIP21/caveolin into liposomes. Surprisingly, the protein reconstituted only with cholesterol-containing lipid mixtures. We demonstrated that the protein binds at least 1 mol of cholesterol per mole of protein and that this binding promotes formation of protein oligomers. These findings suggest that VIP21/caveolin, through its cholesterol-binding properties, serves a specific function in microdomain formation during membrane trafficking. |
| Virion-associated cholesterol is critical for the maintenance of HIV-1 structure and infectivity Campbell, S. M., S. M. Crowe, et al. (2002), Aids 16(17): 2253-61. Abstract: OBJECTIVE: HIV-1 particles are enriched with cholesterol; however, the significance of this cholesterol enrichment is unknown. This study examines the structural and functional roles of cholesterol in HIV-1 replication. METHODS: Using methyl-beta-cyclodextrin (CD) to remove cholesterol from the HIV-1 envelope, buoyant density and infectivity of the cholesterol-deficient HIV-1 particles were compared with the untreated control. The specificity and requirement of cholesterol as an HIV-1-associated lipid were investigated by replenishing cholesterol-deficient HIV-1 with cholesterol, cholestenone (a cholesterol structural analogue) or sphingomyelin (a structurally unrelated yet virion-associated lipid). RESULTS: CD-mediated removal of virion cholesterol increased the buoyant density of virion particles and reduced HIV-1 infectivity. Trans-supplementation of exogenous cholesterol rescued the defects associated with CD-induced cholesterol depletion in HIV-1. However, the restoration of viral infectivity could not be achieved by trans-supplementation of either cholestenone or sphingomyelin. CONCLUSION: This study provides the first direct evidence that HIV-1-associated cholesterol is important for the maintenance of virion structure and infectivity. While the buoyant density of cholesterol-defective HIV-1 can be restored by a cholesterol structural analogue, cholestenone, the requirement for cholesterol is essential for HIV-1 infectivity. |
| Visceral obesity attenuates the effect of the hepatic lipase -514C>T polymorphism on plasma HDL-cholesterol levels in French-Canadian men St-Pierre, J., I. Miller-Felix, et al. (2003), Mol Genet Metab 78(1): 31-6. Abstract: The dyslipidemic state of visceral obesity is characterized by increased plasma triglyceride (TG) levels, low HDL-cholesterol concentrations and alterations in LDL composition and concentration. A functional, non-coding -514C>T single nucleotide polymorphism (SNP) of the hepatic lipase gene (LIPC) has been related to variation in HDL-cholesterol concentrations. OBJECTIVES: To investigate the hypotheses that the LIPC -514C>T polymorphism may be associated with a deteriorated lipoprotein-lipid profile and that environmental factor, such as abdominal obesity, alters this association. METHODS: A total of 235 French-Canadian men from the greater Quebec City area were assigned into three groups on the basis of their LIPC -514C>T SNP, including 149 CC homozygotes, 75 CT heterozygotes, and 11 TT homozygotes. RESULTS: In the present study, the highest values of BMI, waist circumference, and accumulation of visceral adipose tissue (VAT) were observed among TT homozygotes (p<0.05). After adjustment for age and BMI, TT homozygotes still showed higher plasma apolipoprotein (apo) AI and HDL-TG concentrations than the two other groups (p<0.05). When the two genotype groups (CC vs CT/TT) were further divided on the basis of VAT accumulation using a cut-off point of 130 cm(2) (high vs low) it appears that irrespective of the genotype subjects with low VAT had higher HDL(2)-cholesterol concentrations (p<0.0001). However, lean carriers of the T allele had higher plasma HDL(2)-cholesterol levels than lean CC homozygotes. The beneficial effect of the T allele on plasma HDL(2)-cholesterol levels was abolished in the presence of visceral obesity (VAT>130 cm(2)).CONCLUSION: In summary, the presence of visceral obesity attenuates the impact of the LIPC -514C>T polymorphism on plasma HDL(2)-cholesterol levels. |
| Visible-light-harvesting organogel composed of cholesterol-based perylene derivatives Sugiyasu, K., N. Fujita, et al. (2004), Angew Chem Int Ed Engl 43(10): 1229-33. |
| Visualization of a covalent intermediate between microsomal epoxide hydrolase, but not cholesterol epoxide hydrolase, and their substrates Muller, F., M. Arand, et al. (1997), Eur J Biochem 245(2): 490-6. Abstract: Mammalian soluble and microsomal epoxide hydrolases have been proposed to belong to the family of alpha/beta-hydrolase-fold enzymes. These enzymes hydrolyse their substrates by a catalytic triad, with the first step of the enzymatic reaction being the formation of a covalent enzyme-substrate ester. In the present paper, we describe the direct visualization of the ester formation between rat microsomal epoxide hydrolase and its substrate. Microsomal epoxide hydrolase was precipitated with acetone after brief incubation with 1-(14)Cepoxystearic acid. After denaturing SDS gel electrophoresis the protein-bound radioactivity was detected by fluorography. Pure epoxide hydrolase and crude microsomes showed a single radioactive signal of the expected molecular mass that could be suppressed by inclusion of the competitive inhibitor 1,1,1-trichloropropene oxide in the incubation mixture. In a similar manner, 4-fluorochalcone-oxide-sensitive binding of epoxystearic acid to rat soluble epoxide hydrolase could be demonstrated in rat liver cytosol. Under similar conditions, no covalent binding of 26-(14)Ccholesterol-5alpha,6alpha-epoxide to microsomal proteins or solubilized fractions tenfold enriched in cholesterol epoxide hydrolase activity could be observed. Our data provide definitive proof for the formation of an enzyme-substrate-ester intermediate formed in the course of epoxide hydrolysis by microsomal epoxide hydrolase, show no formation of a covalent intermediate between cholesterol epoxide hydrolase and its substrate under the same conditions as those under which an intermediate was shown for both microsomal and soluble epoxide hydrolases and therefore indicate that the cholesterol epoxide hydrolase apparently does not act by a similar mechanism and is probably not structurally related to microsomal and soluble epoxide hydrolases. |
| Visualization of lateral phases in cholesterol and phosphatidylcholine monolayers at the air/water interface--a comparative study with two different reporter molecules Slotte, J. P. and P. Mattjus (1995), Biochim Biophys Acta 1254(1): 22-9. Abstract: This study has compared two chemically distinct NBD-lipids with regard to their partitioning properties into lateral phases of pure and mixed cholesterol/phosphatidylcholine monolayers. Pure NBD-cholesterol (22-(N-(7-nitrobenz-2-oxa-1,3-diazol-4-yl)amino)-23,24-bisnor++ +-5-cholen-3-ol), which has the NBD-function in the sterol side chain (at carbon 22), gave a liquid-expanded force-area isotherm on water at 22 degrees C (having a compressibility of 0.005 to 0.007 m/mN), although epifluorescence microscopy of the compressed NBD-cholesterol monolayer revealed that it had a solid-like surface texture. When the compressed NBD-cholesterol monolayer was allowed to expand, it fragmented into large flakes (tens to hundreds of microns in width) which eventually dissolved into a liquid state. The force-area isotherm of pure NBD-phosphatidylcholine (1-hexadecanoyl-2-(12-(7-nitrobenz-2-oxa-1,3-diazol-4-yl)amino)dod ecyl-sn- glycero-3-phosphocholine) was also liquid-expanded. When a compressed (30 mN/m) monolayer of NBD-phosphatidylcholine was examined by microscopy, it displayed many bright crystalline spots (about 50 microns across) which appeared to form when the monolayer was allowed to stabilize at this lateral surface pressure. These bright spots disappeared when the monolayer was expanded. When the surface texture of a pure cholesterol monolayer was examined, both probes (at 1 mol%) partitioned very similarly in the sterol monolayer. At low lateral surface pressures (1 and 5 mN/m) the probes appeared to be excluded from the cholesterol phase, forming very bright liquid-like areas against a uniformly black cholesterol phase. At 30 mN/m, NBD-phosphatidylcholine appeared to distribute increasingly into the cholesterol phase, whereas NBD-cholesterol still did not to mix with cholesterol. The characteristic surface texture of the liquid-expanded to liquid-condensed lateral phase transition of pure dipalmitoyl phosphatidylcholine (DPPC) monolayers could be visualized identically with both probes, indicating that these were similarly excluded from the liquid-condensed solid phase of DPPC. Finally, in mixed monolayers containing cholesterol and DPPC (molar ratio 33:67), both probes (at 1 mol%) revealed a similar surface texture of the monolayers (examined at a lateral surface pressure of 0.5 mN/m), suggesting that these partitioned similarly between the different lateral phases present in the mixed monolayer. In conclusion, although the two NBD-probes differed from each other in chemical and physical properties, both acted like 'impurities' when admixed into pure or mixed monolayers, and appeared to be equally excluded from lateral phases in which the packing density was high. |
| Visualizing caveolin-1 and HDL in cholesterol-loaded aortic endothelial cells Chao, W. T., S. S. Fan, et al. (2003), J Lipid Res 44(6): 1094-9. Abstract: Caveolae are vesicular invaginations of the plasma membranes that regulate signal transduction and transcytosis, as well as cellular cholesterol homeostasis. Our previous studies indicated that the removal of cholesterol from aortic endothelial cells and smooth muscle cells in the presence of HDL is associated with plasmalemmal invaginations and plasmalemmal vesicles. The goal of the present study was to investigate the location and distribution of caveolin-1, the main structural protein component of caveolae, in cholesterol-loaded aortic endothelial cells after HDL incubation. Confocal microscopic analysis demonstrated that the caveolin-1 appeared to colocalize with HDL-fluorescein 1,1'-dioctadecyl 3,3,3',3'-tetramethylindocarbocyanine perchlorate (DiI) conjugates on the cell surface. No free HDL-DiI conjugates were revealed in the cytoplasm. Immunoelectron microscopy further demonstrated that caveolin-1 gold (15 nm) conjugates colocalized with HDL gold (10 nm) conjugates in the plasmalemmal invaginations. These morphological results indicated that caveolae are the major membrane domains facilitating the transport of excess cholesterol to HDL on the cell surface of aortic endothelial cells. |
| Vitamin C and plasma cholesterol Hemila, H. (1992), Crit Rev Food Sci Nutr 32(1): 33-57. |
| Vitamin C reduces cholesterol-induced microcirculatory changes in rabbits Freyschuss, A., R. J. Xiu, et al. (1997), Arterioscler Thromb Vasc Biol 17(6): 1178-84. Abstract: The microcirculation was studied for 10 weeks in untreated rabbits (n = 12) and in rabbits treated with vitamin C in their drinking water (0.5 g/d; n = 6), a 1% cholesterol diet (n = 12), or a combination of the two treatments (n = 11). The studies were performed by direct intravital microscopic imaging of the conjunctiva of both eyes to evaluate blood flow velocity, microvessel diameter, and microhemorheologic conditions. As we reported previously, changes occurred in all of the aforementioned variables as a consequence of cholesterol feeding. After 3 and 6 weeks of feeding, there was a marked and significant (P <.0001) decrease in blood flow velocity in third-order arterioles, which was accompanied by stasis and erythrocyte aggregation in the smaller conjunctival vessels. When cholesterol treatment was combined with vitamin C, blood flow was almost identical to that of controls and significantly (P <.0001) higher than that of rabbits treated with cholesterol alone. All other changes were also significantly reduced by the addition of vitamin C treatment to the cholesterol diet. Cholesterol-treated rabbits developed macroscopic arterial lesions that were not significantly reduced by vitamin C treatment. Neither circulating oxysterol levels nor atheromas were reduced by vitamin C treatment, which also had no significant effect on lipid or circulating vitamin E levels. We have previously shown that the lipid-soluble antioxidant BHT is able to prevent both cholesterol-induced microcirculatory changes and the development of arterial lesions in rabbits. This phenomenon is compatible with a critical oxidation step occurring in the lipid phase that is common to both processes. The finding that microcirculatory changes can be prevented by a water-soluble antioxidant is compatible with a role for water-soluble oxidants in this context. The possibility is discussed that vitamin C might also be important for the microcirculation in humans. |
| Vitamin C, cholesterol, and the nutritional recommendations Hemila, H. (1993), Am J Cardiol 71(5): 503-4. |
| Vitamin D is a membrane antioxidant. Ability to inhibit iron-dependent lipid peroxidation in liposomes compared to cholesterol, ergosterol and tamoxifen and relevance to anticancer action Wiseman, H. (1993), FEBS Lett 326(1-3): 285-8. Abstract: Vitamin D is a membrane antioxidant: thus Vitamin D3 (cholecalciferol) and its active metabolite 1,25-dihydroxycholecalciferol and also Vitamin D2 (ergocalciferol) and 7-dehydrocholesterol (pro-Vitamin D3) all inhibited iron-dependent liposomal lipid peroxidation. Cholecalciferol, 1,25-dihydroxycholecalciferol and ergocalciferol were all of similar effectiveness as inhibitors of lipid peroxidation but were less effective than 7-dehydrocholesterol; this was a better inhibitor of lipid peroxidation than cholesterol, though not ergosterol. The structural basis for the antioxidant ability of these Vitamin D compounds is considered in terms of their molecular relationship to cholesterol and ergosterol. Furthermore, the antioxidant ability of Vitamin D is compared to that of the anticancer drug tamoxifen and its 4-hydroxy metabolite (structural mimics of cholesterol) and discussed in relation to the anticancer action of this vitamin. |
| Vitamin E and factors affecting atherosclerosis in rabbits fed a cholesterol-rich diet Ismail, N. M., N. Abdul Ghafar, et al. (2000), Int J Food Sci Nutr 51 Suppl: S79-94. Abstract: The present study aims to examine the effects of a palm-oil-derived vitamin E mixture containing tocotrienol (approximately 70%) and tocopherol (approximately 30%) on plasma lipids and on the formation of atherosclerotic plaques in rabbits given a 2% cholesterol diet. Eighteen New Zealand White rabbits (2.2-2.8 kg) were divided into three groups; group 1 (control) was fed a normal diet, group 2 (AT) was fed a 2% cholesterol diet and group 3 (PV) was fed a 2% cholesterol diet with oral palm vitamin E (60 mg/kg body weight) given daily for 10 weeks. There were no differences in the total cholesterol and triacylglycerol levels between the AT and PV groups. The PV group had a significantly higher concentrations of HDL-c and a lower TC/HDL-c ratio compared to the AT group (P < 0.003). The aortic tissue content of cholesterol and atherosclerotic lesions were comparable in both the AT and PV groups. However, the PV group had a lower content of plasma and aortic tissue malondialdehyde (P < 0.005). Our findings suggest that despite a highly atherogenic diet, palm vitamin E improved some important plasma lipid parameters, reduced lipid peroxidation but did not have an effect on the atherosclerotic plaque formation. |
| Vitamin E and vitamin A concentrations in plasma adjusted for cholesterol and triglycerides by multiple regression Jordan, P., D. Brubacher, et al. (1995), Clin Chem 41(6 Pt 1): 924-7. Abstract: The plasma concentration of vitamins A and E varies with the amount of concurrent lipids and thus requires lipid standardization. The present study compares a new multiple regression-based method for adjusting vitamins A and E concentrations for cholesterol and triglycerides with previous methods (adjustment for cholesterol only, and adjustment for the sum of cholesterol and triglycerides). The results show that the new method can reduce influence of the concurrent lipids. |
| Vitamin E combined with selenium inhibits atherosclerosis in hypercholesterolemic rabbits independently of effects on plasma cholesterol concentrations Schwenke, D. C. and S. R. Behr (1998), Circ Res 83(4): 366-77. Abstract: Several antioxidants inhibit atherosclerosis. This study investigated the hypothesis that combining vitamin E, a lipophilic antioxidant, with vitamin C, a hydrophilic antioxidant, and/or selenium, a cofactor of peroxidases that detoxify lipid peroxides, would inhibit atherosclerosis more effectively than vitamin E alone. We also considered whether regional variation in inhibition of atherosclerosis by antioxidants would be associated with regional variation in aortic lipophilic antioxidants. Rabbits were fed an atherogenic diet (control) or an atherogenic diet supplemented with vitamin E, vitamins E and C, vitamin E+selenium, vitamins E and C+selenium, or probucol (positive control). Supplements were as follows: vitamin E, 146 IU/d; vitamin C, 791 mg/d; selenium, 22 microg/d; or probucol, 406 mg/d. Vitamin C did not influence atherosclerosis. After 22 weeks of treatment, rank order of aortic atherosclerosis was control>vitamin E (with or without vitamin C)>vitamin E+selenium (with or without vitamin C)>probucol. Antioxidant treatment reduced aortic cholesterol concentrations 21% to 56%, 29% to 86%, and 19% to 75% for the aortic arch, descending thoracic aorta, and abdominal aorta, respectively (P<0.025 to P<0.0003 by ANOVA), with slightly greatly reductions for areas of atherosclerotic lesions. Some treatments reduced plasma cholesterol concentrations, but none altered the distribution of cholesterol among lipoproteins. Corrected for differences in plasma cholesterol concentrations, aortic cholesterol concentrations were reduced up to 72% (P<0.02) by the antioxidant treatments, with equal reductions by vitamin E+selenium and by probucol. Aortic alpha-tocopherol standardized by aortic cholesterol as a measure of aortic lipids was lower in the abdominal aorta than in the aortic arch of rabbits not given alpha-tocopherol and increased relatively more in the abdominal aorta than in the aortic arch with alpha-tocopherol supplementation. The results of this study suggest that vitamin E+ selenium inhibited atherosclerosis as effectively as an equally hypocholesterolemic dose of probucol by a mechanism(s) that is in part independent of effects on plasma and lipoprotein cholesterol concentrations. The tendency for greater efficacy of antioxidant treatments in the abdominal aorta than aortic arch may relate to the lower concentrations of alpha-tocopherol in the abdominal aorta of unsupplemented rabbits. |
| Vitamin E inhibits the intimal response to balloon catheter injury in the carotid artery of the cholesterol-fed rat Konneh, M. K., C. Rutherford, et al. (1995), Atherosclerosis 113(1): 29-39. Abstract: We have investigated the effect of the naturally occurring, lipid-soluble antioxidant, vitamin E, on the intimal response to balloon injury in the cholesterol-fed rat. We found that in animals receiving a 0.5% vitamin E plus 1% cholesterol diet, neo-intimal thickening was reduced by 30% (P < 0.025) compared to animals receiving either cholesterol alone, or a control chow diet. In all three dietary groups, the intimal lesion consisted predominantly of smooth muscle cells, and few monocytes/macrophages (< 0.5%) could be identified by staining with the monoclonal antibody ED-1. In vitro, vitamin E inhibited platelet-derived growth factor- (PDGF) (20 ng/ml) and serum (2%)-induced mitogenesis of both adult rat thoracic aortic smooth muscle cells and an embryonic rat aortic smooth muscle cell line (A7r5), dose-dependently. These data suggest that reactive oxygen species may be involved in the intimal response to balloon catheter injury, and that antioxidants, such as vitamin E, may offer some protection against restenosis. Although the way by which it does so is unclear, one possible mechanism is by a direct inhibitory effect on the accumulation of smooth muscle cells within the developing neo-intima. |