| For medical practitioners and the general public - Cholesterol Journal Article Catalog. |
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| Cholesterol crystals in gouty bursitis Fam, A. G. (2001), J Rheumatol 28(8): 1928-9. |
| Cholesterol crystals in hydroceles: sonographic detection and possible significance Gooding, G. A., W. C. Leonhardt, et al. (1997), AJR Am J Roentgenol 169(2): 527-9. Abstract: OBJECTIVE: The aim of this study of seven patients who had elective surgical repairs of a hydrocele was to try to differentiate by microscopy and chemical analysis hyperechoic hydrocele fluid from the more typical anechoic hydrocele fluid. CONCLUSION: Hyperechoic hydrocele fluid is related to the presence of cholesterol crystals. Cholesterol crystals were noted on microscopic examination in all three patients with hyperechoic hydrocele fluid. No cholesterol crystals were evident in the four patients with typical anechoic hydrocele fluid. |
| Cholesterol crystals in synovial and bursal fluid Lazarevic, M. B., J. L. Skosey, et al. (1993), Semin Arthritis Rheum 23(2): 99-103. Abstract: Cholesterol crystals were found in two patients with classic rheumatoid arthritis (RA). In one patient, cholesterol crystals were found in synovial fluid from both shoulder joints, and in the second they were in an olecranon bursa. To examine the possible systemic etiology of cholesterol crystals in synovial and bursal fluid, lipid concentrations and the presence of serum antilipoprotein antibodies were measured. Antilipoprotein antibodies were not found. The concentration of lipid and lipoproteins, as well as the normal pattern of lipoprotein on agarose gel, eliminates the possibility of hyperlipoproteinemia. Results seemed to exclude a systemic etiology for the formation of cholesterol crystals in synovial and bursal fluid in the RA patients. It appears that several local factors such as defective drainage, local destruction, increased permeability of synovial membrane, and intraarticular (bursal) bleeding are possible etiologies. |
| Cholesterol crystals pericarditis Jimenez Elorza, A., P. M. Montes Orbe, et al. (2001), Rev Esp Cardiol 54(9): 1119-20. Abstract: Cholesterol pericarditis is an uncommon, specific form of pericardial disease that is characterized by the presence of cholesterol crystals in pericardial fluid. The etiology may be either idiopathic or in association with systemic disorders such as tuberculosis, rheumatoid arthritis, myxedema or hypercholesterolemia. We report a case of cholesterol pericarditis in a 51-year-old male who was diagnosed with chronic renal failure due to polycystic kidney disease. To our knowledge no similar cases have been reported to date in the literature. |
| Cholesterol crystals, smooth muscle cells and new data on the genesis of atherosclerosis Kiyak, J. H. (1997), Pol J Pathol 48(1): 49-55. Abstract: The histologic appearance of atherosclerosis has been well described but its pathogenesis is still vigorously debated. The purpose of the present study is to clarify the stimuli for smooth muscle cells (SMC) migration and proliferation as well as the way of cholesterol crystals (CC) generation. We performed postmortem ultrastructural analysis of myocardial samples obtained from 45 patients (33 males, 12 females, age range 18-85) who died from different diseases, mainly from acute myocardial infarction-MI (37 cases). Tissue was taken by transthorax express-necropsy method immediately after patients' death in the clinic. In myocardial infarction cases intact zones of the heart were examined. We have found a few foci of modified SMC proliferation in the periarteriolar space around necrotic cellular debris in elder patients. Lymphocytes, myofibroblasts and some leukocytes infiltrated those areas. The modified SMC phagocyted necrotic material and formed secondary lysosomes, inside which from one to three CC originated. In parallel with the reduction of necrotic mass inside the lysosomes, CC size increased. In the final phase the CC were discharged from the SMC into the interstitium. After exocytosis a tendency for the CC to accumulate was observed. They formed clusters consisting of 20-30 crystals. Most of the CC were of typical needle-like or rhomboid shape. Modified SMC were producing not only CC but also collagen and elastin. This study indicates that atherosclerotic process in the myocardium is connected with the appearance of modified SMC inside which CC are generated. |
| Cholesterol cyst and cholesterol granuloma of the petrous bone Morrison, G. A. and M. G. Dilkes (1992), J Laryngol Otol 106(5): 465-7. |
| Cholesterol cysts of the petrous apex: radiological evaluation and surgical management Breidahl, W. H., C. P. Bracks, et al. (1992), Aust N Z J Surg 62(6): 429-35. Abstract: The clinical presentation, diagnostic features and surgical management of three cases of giant cholesterol cysts involving the petrous apex of the temporal bone are presented. The ability to reach a confident pre-operative diagnosis using magnetic resonance imaging (MRI) due to its greater soft tissue contrast resolution, multiplanar imaging capabilities and sensitivity to blood products is illustrated. The operation of transmastoid infralabyrinthine draining of the petrous apex is described and other possible approaches discussed. |
| Cholesterol cysts of the temporal bone: diagnosis and treatment Goldofsky, E., R. A. Hoffman, et al. (1991), Ann Otol Rhinol Laryngol 100(3): 181-7. Abstract: Cholesterol cyst (or granuloma) of the temporal bone, a recognized clinical entity distinct from cholesteatoma, is more common than previously thought. Apparently it is caused by obstruction of previously pneumatized temporal bone air cells. Surgical cure is achieved by drainage and reestablishment of normal pneumatization. This paper reviews 14 cholesterol cysts of the temporal bone, emphasizing the importance of preoperative imaging and surgical approach. Use of magnetic resonance imaging differentiates cholesterol cysts from cholesteatoma or other neoplasms. Computed tomography delineates the location of the lesion and defines temporal bone anatomy essential to surgical approach. The two studies together allow the surgeon to properly plan drainage, as in the case of a cholesterol cyst, versus excision or exteriorization, as in the case of cholesteatoma. The infralabyrinthine approach to a petrous apex cholesterol cyst is the procedure of choice when hearing preservation is desired. |
| Cholesterol cytochemistry in cell biology and disease Severs, N. J. (1997), Subcell Biochem 28: 477-505. |
| Cholesterol debate: evaluation of overeating and lack of exercise as health risk factors? Seiffert, U. (1995), Dtsch Med Wochenschr 120(6): 190-3. |
| Cholesterol decreases secretion of the secreted form of amyloid precursor protein by interfering with glycosylation in the protein secretory pathway Galbete, J. L., T. R. Martin, et al. (2000), Biochem J 348 Pt 2: 307-13. Abstract: Cerebral deposits of beta-amyloid (betaA) are a major feature in Alzheimer's disease. betaA is derived from amyloid precursor protein (APP). APP is subject to N- and O-glycosylation and undergoes a series of proteolytic cleavages that lead to the release of betaA or of a non-amyloidogenic secreted form of APP (APPs). We used primary neuronal and glial cultures to investigate how cholesterol affects the production and secretion of APPs. Exposure to cholesterol for 2 h did not change the neuronal release of APPs; after 6 h APPs release was slightly lower, whereas 24 h of exposure decreased APPs in the medium by approx. 60%. The time courses were similar in astrocytes and microglia preparations. To verify whether the effect of cholesterol was a consequence of membrane rigidification we tested the activity of ganglioside GM1 and prion protein fragment PrP 106-126, which affect membrane fluidity similarly to cholesterol, on APPs secretion. Neither altered the production of APPs. APP mRNA and the total amount of APP in the cells were slightly decreased by cholesterol after 2 and 24 h respectively. Immunoblot analysis of APP associated with neuronal cells and astrocytes indicated that cholesterol progressively decreased the glycosylated forms of the protein; a similar tendency was noted in cells treated with brefeldin A and monensin, two substances that interfere with protein glycosylation. The cell-surface biotinylation method showed that in cholesterol-treated cells APP reached the plasma membrane. Our results indicate that cholesterol decreases the secretion of APPs by interfering with APP maturation and inhibiting glycosylation of the protein; although APP is inserted in the membrane it is not cleaved by alpha-secretase. |
| Cholesterol decreases the interfacial elasticity and detergent solubility of sphingomyelins Li, X. M., M. M. Momsen, et al. (2001), Biochemistry 40(20): 5954-63. Abstract: The interfacial interactions of cholesterol with sphingomyelins (SMs) containing various homogeneous acyl chains have been investigated by Langmuir film balance approaches. Low in-plane elasticity among the packed lipids was identified as an important physical feature of the cholesterol-sphingomyelin liquid-ordered phase that correlates with detergent resistance, a characteristic property of sphingolipid-sterol rafts. Changes in the in-plane elastic packing, produced by cholesterol, were quantitatively assessed by the surface compressional moduli (C(s)(-1)) of the monolayer isotherms. Of special interest were C(s)(-1) values determined at high surface pressures (>30 mN/m) that mimic the biomembrane situation. To identify structural features that uniquely affect the in-plane elasticity of the sphingomyelin-cholesterol lateral interaction, comparisons were made with phosphatidylcholine (PC)-cholesterol mixtures. Cholesterol markedly decreased the in-plane elasticity of either SM or PC regardless of whether they were fluid or gel phase without cholesterol. The magnitude of the reduction in in-plane elasticity induced by cholesterol was strongly influenced by acyl chain structure and by interfacial functional groups. Liquid-ordered phase formed at lower cholesterol mole fractions when SM's acyl chain was saturated rather than monounsaturated. At similar high cholesterol mole fractions, the in-plane elasticity within SM-cholesterol liquid-ordered phase was significantly lower than that of PC-cholesterol liquid-ordered phase, even when PCs were chain-matched to the SMs. Sphingoid-base functional groups (e.g., amide linkages), which facilitate or strengthen intermolecular hydrogen bonds, appear to be important for forming sphingomyelin-cholesterol, liquid-ordered phases with especially low in-plane elasticity. The combination of structural features that predominates in naturally occurring SMs permits very effective resistance to solubilization by Triton X-100. |
| Cholesterol defect in Smith-Lemli-Opitz syndrome Tint, G. S. (1993), Am J Med Genet 47(4): 573-4. |
| Cholesterol deficiency increases the vulnerability of hippocampal glia in primary culture to glutamate-induced excitotoxicity Chou, Y. C., S. B. Lin, et al. (2003), Neurochem Int 43(3): 197-209. Abstract: Cholesterol, a molecule critical for cellular function, is found in particular high concentration in the brain and has been implicated to synaptic plasticity and neuronal regeneration. This study was undertaken to investigate the mechanism by which cholesterol shortage modulates glutamate (Glu)-induced excitotoxicity in hippocampal cell cultures. A combined treatment of lovastatin and beta-cyclodextrin reduced cellular content of cholesterol while having no significant effect on cell viability in neuron/glia mixed cultures. The experimental manipulation, nonetheless, exacerbated Glu-induced membrane damage and loss of mitochondrial activity in mixed cultures. Analysis of 3Hthymidine incorporation revealed cholesterol deficiency impaired cell proliferation in mixed cultures after Glu exposure, indicating considerable loss of glia. Indeed, it was found that cholesterol deprivation potentiated the release of lactate dehydrogenase (LDH) and the impairment in mitochondrial reduction of WST-1 reagent in astrocyte-enriched cultures subjected to Glu exposure. The detrimental effect of cholesterol shortage, nevertheless, was not observed in cultured neurons. Notably, the pretreatment of lovastatin and beta-cyclodextrin caused a decrease in the content of cellular LDH while having no effect on cell cycle profile and cellular activity of WST-1 reduction in astrocyte-enriched cultures. In contrast, removal of cholesterol had no effect on LDH content in neuron-enriched cultures. It is concluded that the differential vulnerability of cholesterol-depleted neural cells to excitotoxic damage may, in part, be ascribed to cholesterol shortage destabilizing the plasma membrane of astrocytes, thus rendering them less capable of withstanding Glu insult. |
| Cholesterol deficit but not accumulation of aberrant sterols is the major cause of the teratogenic activity in the Smith-Lemli-Opitz syndrome animal model Gaoua, W., C. Wolf, et al. (2000), J Lipid Res 41(4): 637-46. Abstract: Low cholesterol and high 7-dehydrocholesterol (7DHC) levels are associated with a blockade of Delta7-reductase in the Smith-Lemli-Opitz syndrome (SLOS) and in the animals treated with the inhibitor AY9944. The impact of the cholesterol deficit and of the accumulation of 7DHC on the embryo were investigated in AY9944-treated pregnant rats receiving an enriched cholesterol or 7DHC diet. Sterol profiling was performed under the various nutritional conditions. AY9944 caused a severe decrease in the maternal and embryo cholesterol. The deficit in the embryo was sustained by the embryonic uptake of the inhibitor. A cholesterol-rich diet was efficient in restoring the maternal and embryonic cholesterol and phenotype but a 7DHC-rich diet did not modify the sterol status compared with dams treated with only AY9944. The offspring phenotype remained deleterious whether or not the dams received 7DHC-rich diet. Over 80% of the 7DHC was absorbed, as was cholesterol, which was not quantitatively influenced by AY9944. When cholesterol and 7DHC were simultaneously administered, a competition for intestinal absorption enhanced the lowering cholesterol effect of AY9944.Whether or not the dams received a 7DHC dietary supplement, the offspring's phenotype became normal when the diet was supplemented with cholesterol. Under conditions in which the ratio of cholesterol/7DHC is substantially varied, the normal development of embryos can be achieved as long as the cholesterol is sufficient. The phenotype is reversed in vivo by cholesterol which contrasts with the irreversible effects manifested in vitro by oxidized 7DHC by-products. |
| Cholesterol delivered to macrophages by oxidized low density lipoprotein is sequestered in lysosomes and fails to efflux normally Dhaliwal, B. S. and U. P. Steinbrecher (2000), J Lipid Res 41(10): 1658-65. Abstract: Oxidized low density lipoprotein (LDL) has been found to exhibit numerous potentially atherogenic properties, including transformation of macrophages to foam cells. It is believed that high density lipoprotein (HDL) protects against atherosclerosis by removing excess cholesterol from cells of the artery wall, thereby retarding lipid accumulation by macrophages. In the present study, the relative rates of HDL-mediated cholesterol efflux were measured in murine resident peritoneal macrophages that had been loaded with acetylated LDL or oxidized LDL. Total cholesterol content of macrophages incubated for 24 h with either oxidized LDL or acetylated LDL was increased by 3-fold. However, there was no release of cholesterol to HDL from cells loaded with oxidized LDL under conditions in which cells loaded with acetylated LDL released about one-third of their total cholesterol to HDL. Even mild degrees of oxidation were associated with impairment of cholesterol efflux. Macrophages incubated with vortex-aggregated LDL also displayed impaired cholesterol efflux, but aggregation could not account for the entire effect of oxidized LDL. Resistance of apolipoprotein B (apoB) in oxidized LDL to lysosomal hydrolases and inactivation of hydrolases by aldehydes in oxidized LDL were also implicated. The subcellular distribution of cholesterol in oxidized LDL-loaded cells and acetylated LDL-loaded cells was investigated by density gradient fractionation, and this indicated that cholesterol derived from oxidized LDL accumulates within lysosomes. Thus impairment of cholesterol efflux in oxidized LDL-loaded macrophages appears to be due to lysosomal accumulation of oxidized LDL rather than to impaired transport of cholesterol from a cytosolic compartment to the plasma membrane. |
| Cholesterol demystified Julien, M. G. (1992), J Dent Que 29: 9-13. Abstract: A favorite subject of newspapers, periodicals or television programs, is that cholesterol has invaded our lives. Although well known as being undesirable, for blocking the arteries and contributing to cardiovascular diseases which kill thousands of Canadians each year, the flood of information of diverse quality leaves most of us puzzled. This paper aims to answer the main questions about cholesterol, trying to better define its relationship to cardiovascular diseases and to provide useful dietary advice to help control this risk factor. |
| Cholesterol dependence of HTLV-I infection Wielgosz, M. M., D. A. Rauch, et al. (2005), AIDS Res Hum Retroviruses 21(1): 43-50. Abstract: Cholesterol-rich plasma membrane microdomains are important for entry of many viruses, including retroviruses. Depletion of cholesterol with 2-hydroxypropyl-beta-cyclodextrin inhibits entry of human T cell leukemia virus type I (HTLV-1) and HTLV-I envelope pseudotyped lentivirus particles. Using a soluble fusion protein of the HTLV-I surface envelope protein with the immunoglobulin Fc domain, the HTLV-I receptor was found to colocalize with a raft-associated marker and to cluster in specific plasma membrane microdomains. Depletion of cholesterol did not alter receptor binding activity, suggesting a requirement for cholesterol in a postbinding virus entry step. |
| Cholesterol dependence of vascular ERK1/2 activation and growth in response to stretch: role of endothelin-1 Zeidan, A., J. Broman, et al. (2003), Arterioscler Thromb Vasc Biol 23(9): 1528-34. Abstract: OBJECTIVE: Stretch-induced growth of the vascular wall plays a role in hypertension and neointima formation. Its signal pathways involve integrins, cytoskeleton, membrane receptors, and ion channels, some of which are organized in cholesterol-rich, membrane domains such as lipid rafts or caveolae. This study tested the role of rafts/caveolae in stretch-induced vascular growth by manipulation of membrane cholesterol contents. METHODS AND RESULTS: Growth and protein synthesis were induced by mechanical stretch of rat portal veins in vitro. Sucrose gradient centrifugation showed stretch-induced tyrosine phosphorylation primarily in fractions containing caveolin-1. Disruption of membrane caveolae with use of methyl-beta-cyclodextrin (mbetacd) reduced weight gain, protein synthesis, and DNA synthesis to levels in unstretched, control veins. These effects were partially reversed by restoration of cellular cholesterol contents. Inhibited growth was associated with abolished activation of extracellular signal-regulated kinase (ERK) 1/2 in response to stretch and endothelin-1 (ET-1) but not to angiotensin II. Inhibition of ET-1 type A (ETA) receptors by RF139317 or endothelin-converting enzyme by phosphoramidone abolished stretch-induced ERK1/2 activation, which was, however, unaffected by removal of the endothelium. CONCLUSIONS: Stretch-induced growth signaling in vascular smooth muscle depends on cholesterol-rich, membrane microdomains by a mechanism involving ETA receptors that respond to endogenous ET-1 production. |
| Cholesterol dependent recruitment of di22:6-PC by a G protein-coupled receptor into lateral domains Polozova, A. and B. J. Litman (2000), Biophys J 79(5): 2632-43. Abstract: Bovine rhodopsin was reconstituted into mixtures of didocosahexaenoylphosphatidylcholine (di22:6-PC), dipalmitoylphosphatidylcholine (di16:0-PC), sn-1-palmitoyl-sn-2-docosahexaenoylphosphatidylcholine (16:0, 22:6-PC) and cholesterol. Rhodopsin denaturation was examined by using high-sensitivity differential scanning calorimetry. The unfolding temperature was increased at lower levels of lipid unsaturation, but the highest temperature was detected for native disk membranes: di22:6-PC < 16:0,22:6-PC < di16:0,18:1-PC < native disks. The incorporation of 30 mol% of cholesterol resulted in 2-4 degrees C increase of denaturation temperature in all reconstituted systems examined. From the analysis of van't Hoff's and calorimetric enthalpies, it was concluded that the presence of cholesterol in di22:6-PC-containing bilayers induces a level of cooperativity in rhodopsin unfolding. Fluorescence resonance energy transfer (FRET), using lipids labeled at the headgroup with pyrene (Py) as donors and rhodopsin retinal group as acceptor of fluorescence, was used to study rhodopsin association with lipids. Higher FRET efficiencies detected for di22:6-PE-Py, compared to di16:0-PE-Py, in mixed di22:6-PC-di16:0-PC-cholesterol bilayers, indicate preferential segregation of rhodopsin with polyunsaturated lipids. The effective range of the rhodopsin-lipid interactions facilitating cluster formation exceeds two adjacent lipid layers. In similar mixed bilayers containing no cholesterol, cluster formation was absent at temperatures above lipid phase transition, indicating a crucial role of cholesterol in microdomain formation. |