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PubMed2005

The relative orientation of the lipid and carbohydrate moieties of lipochitooligosaccharides related to nodulation factors depends on lipid chain saturation.

Lipochitooligosaccharides (LCOs) signal the symbiosis of rhizobia with legumes and the formation of nitrogen-fixing root nodules. LCOs 1 and 2 share identical tetrasaccharide scaffolds but different lipid moieties (1, LCO-IV(C16:1[9Z], SNa) and , LCO-IV(C16:2[2E,9Z], SNa)). The conformational behaviors of both LCOs were studied by molecular modeling and NMR. Modeling predicts that a small lipid modification would result in a different relative orientation of the lipid and tetrasaccharide moieties. Diffusion ordered spectroscopy reports that both LCOs form small aggregates above 1 mM. Nuclear Overhauser spectroscopy (NOESY) data, collected under monomeric conditions, reveals lipid-carbohydrate contacts only for 1, in agreement with the modeling data. The distinct molecular structures of 1 and 2 have the potential to contribute to their selective binding by legume proteins.

Carbohydrate Conformation↗
PubMed1992

Effects of organic anions on biliary lipid secretion in rats. Importance of association with biliary lipid structures.

This study was performed to determine the effects of various organic anions on biliary lipid secretion in rats. We infused bile-salt-pool-depleted rats with sodium taurocholate at a constant rate, with or without various organic anions: Indocyanine Green (ICG), bromosulphophthalein (BSP), BSP-glutathione and Phenol Red (PR). BSP decreased biliary secretion of cholesterol and phospholipids in a dose-dependent manner without affecting bile salt secretion (uncoupling), and this change was fully reversible. In contrast, ICG, BSP-glutathione and PR did not cause such an uncoupling of biliary lipids. In addition, the distribution pattern of each organic anion to various lipid particles was determined by gel-permeation chromatography. BSP was predominantly associated with bile salt micelles, whereas vesicular association was dominant for ICG, and both BSP-glutathione and PR formed only self-aggregations. From these data, we concluded that the uncoupling of biliary lipids from bile salt secretion by BSP resulted from the interaction between BSP and bile salt micelles in the bile canaliculus, and that this interaction inhibited the capacity of bile salts to induce the secretion of phospholipids and cholesterol.

Animals↗
PubMed1993

Prospective study of the evaluation of hepatitis C virus infectivity in a high-purity, solvent/detergent-treated factor VIII concentrate: parallel evaluation of other markers for lipid-enveloped and non-lipid-enveloped viruses. The Ad Hoc Study Group of the Fondazione dell'Emofilia.

This prospective study was carried out with the aim of evaluating the efficacy of solvent/detergent inactivation of the hepatitis C virus (HCV) as applied to a chromatographic factor VIII concentrate. In parallel, the markers for other viruses, either lipid-enveloped (human immunodeficiency virus types 1 and 2 [HIV-1 and -2] and hepatitis B virus [HBV]) or non-lipid-enveloped viruses (such as B19 parvovirus and hepatitis A virus [HAV]) were evaluated. The study included 14 hemophilia centers, which enrolled 36 previously untreated patients (median age, 3 years; range, 1-56). The length of follow-up was 12 months, during which HCV (first- and second-generation assays and recombinant immunoblot assay), HIV-1 and -2, HBV, HAV (IgG and IgM), and parvovirus (IgG and IgM) antibodies, as well as alanine aminotransferase values were evaluated. Thirty-one patients were analyzable; none seroconverted for HCV, HBV, or HIV after exposure to a total of 165,000 IU of factor VIII (41 different lots). In one patient, alanine aminotransferase values rose to 167 mU per mL, 6 weeks after the first concentrate infusion, and this patient seroconverted for HAV 1 week later. Furthermore, 10 patients seroconverted for parvovirus during follow-up. This study suggests that the solvent/detergent method of virus inactivation is efficient in relation to lipid-enveloped blood-borne viruses but not in relation to non-lipid-enveloped viruses.

Adolescent↗
PubMed1994

Inactivation of lipid-enveloped and non-lipid-enveloped model viruses in normal human plasma by crosslinked starch-iodine.

BACKGROUND: The purpose of this study was to evaluate an iodine-based method of activating potentially harmful viruses that might be found in normal human plasma. STUDY DESIGN AND METHODS: A procedure has been developed for inactivating lipid-enveloped and non-lipid-enveloped model viruses in normal human plasma by using iodine complexed to crosslinked potato starch. The established conditions are an iodine concentration of 1.05 mg per mL and 60 minutes' incubation. RESULTS: Under these conditions, inactivation of more than 9 log10 of vesicular stomatitis virus, a lipid-enveloped virus, and more than 7 log10 of encephalomyocarditis virus, a non-lipid-enveloped virus, was achieved, with minimal losses of biologic activity of selected plasma proteins. Under these conditions, 70 percent of factor VIII activity, 77 percent of factor IX activity, and 100 percent of protein C activity in the plasma were retained. CONCLUSION: Crosslinked starch-iodine may be useful in the inactivation of viruses in single-donor plasma units and in pooled human plasma before fractionation.

Blood↗
PubMed1998

Lipid patches in membrane protein oligomers: crystal structure of the bacteriorhodopsin-lipid complex.

Heterogenous nucleation on small molecule crystals causes a monoclinic crystal form of bacteriorhodopsin (BR) in which trimers of this membrane protein pack differently than in native purple membranes. Analysis of single crystals by nano-electrospray ionization-mass spectrometry demonstrated a preservation of the purple membrane lipid composition in these BR crystals. The 2.9-A x-ray structure shows a lipid-mediated stabilization of BR trimers where the glycolipid S-TGA-1 binds into the central compartment of BR trimers. The BR trimer/lipid complex provides an example of local membrane thinning as the lipid head-group boundary of the central lipid patch is shifted by 5 A toward the membrane center. Nonbiased electron density maps reveal structural differences to previously reported BR structures, especially for the cytosolic EF loop and the proton exit pathway. The terminal proton release complex now comprises an E194-E204 dyad as a diffuse proton buffer.

Journal Article↗
PubMed2004

Regulated internalization and phosphorylation of the native norepinephrine transporter in response to phorbol esters. Evidence for localization in lipid rafts and lipid raft-mediated internalization.

The effects of norepinephrine in the brain and periphery are terminated primarily by active reuptake of the catecholamine via cocaine- and amphetamine-sensitive norepinephrine transporters (NETs). Activation of protein kinase C (PKC) down-regulates NET by sequestering it from the plasma membrane, although the underlying mechanism is not yet known. Previously, we showed robust expression of endogenous NETs in rat placental trophoblasts (Jayanthi, L. D., Vargas, G., and DeFelice, L. J. (2002) Br. J. Pharmacol. 135, 1927-1934). Here we report a significant reduction in native NET function and surface expression in these cells following phorbol ester (beta-PMA) treatment. The beta-PMA-mediated down-regulation of NET occurs by a rapid sequestration of NETs from the plasma membrane and is calcium-independent. Reversible biotinylation experiments revealed a significant enhancement of NET endocytosis following beta-PMA treatment. Chemical treatments and expression of dominant negative mutants of dynamin 1 and 2 failed to prevent the beta-PMA effect, suggesting a clathrin-independent pathway. In contrast, treatment with the cholesterol-disrupting agent filipin, which blocks caveolae/lipid raft-mediated internalization, completely blocked the beta-PMA-mediated NET sequestration. Discontinuous sucrose density gradient centrifugation revealed NET in the lipid raft fractions. Following beta-PMA treatment, there was reduced NET levels in the lipid raft fractions suggesting that cholesterol-rich lipid rafts mediate PKC-triggered NET internalization. Metabolic labeling and immunoprecipitation studies revealed that NET phosphorylation is stimulated severalfold by PKC activation and protein phosphatase 1/2A inhibition. Together, these findings demonstrate for the first time that in trophoblasts (i) PKC activation regulates NET function and surface expression by an enhanced internalization process that is lipid raft-mediated and (ii) PKC and protein phosphatase(s) modulation regulates NET phosphorylation.

Animals↗
PubMed1987

Drug therapy for lipid disorders. Selecting appropriate lipid-lowering agents.

Lipid abnormalities can be treated effectively with various lipid-lowering agents. However, it bears repeating that no patient with hyperlipidemia should be treated with drugs until an adequate trial of dietary intervention, which may take as long as six months, has been attempted. While knowledge of a patient's precise metabolic and genetic abnormality is often desirable, it generally is not necessary for the institution of lipid-lowering drug therapy. Judicious use of total cholesterol, high-density lipoprotein cholesterol, and total triglyceride measurements is sufficient for selection of the proper drug or drugs. A patient who does not respond should be referred to a specialized lipid center for more sophisticated evaluation and therapy.

Anticholesteremic Agents↗
PubMed1999

Effects of dietary omega-3 and omega-6 lipids and vitamin E on serum cytokines, lipid mediators and anti-DNA antibodies in a mouse model for rheumatoid arthritis.

OBJECTIVE: Omega-3 (omega-3) fatty acid rich-fish oil (FO) and vitamin E (vit-E) may delay the progress of certain autoimmune diseases. The present study examined the mechanism of action of omega-3 and omega-6 lipids and vit-E on the serum cytokines and lipid mediators in autoimmune-prone MRL/lpr mice (a model for rheumatoid arthritis, RA). The lpr (lymphoproliferative) gene is overexpressed in these mice causing extensive lymphoproliferation, lupus-like symptoms and accelerated aging. METHODS: Weanling female MRL/lpr and congenic control MRL/++ mice were fed 10% corn oil (CO, omega6) or FO-based semipurified diets containing two levels of vitamin E (vit-E-75, I.U. and vit-E-500 I.U./Kg diet) for four months. At the end of the experiment, serum anti-DNA antibodies, cytokines and lipid mediators levels were determined. RESULTS: The appearance of enlarged lymph nodes was delayed in the mice fed FO, and the FO-500 IU vit-E diet offered further protection against enlargement of lymph nodes. The MRL/lpr mice exhibited significantly higher levels of serum anti-dsDNA antibodies. The FO-fed mice had significantly lower serum IL-6, IL-10, IL-12, TNF-alpha, PGE2, TXB2 and LTB4 levels compared with CO-fed mice. In mice fed 500 IU vit-E diets, the serum IL-6, IL-10, IL-12 and TNF-alpha levels were significantly lower and serum IL-1beta was significantly higher compared to 75 IU-vit-E-fed mice in CO/FO or both. The levels of anti-DNA antibodies, IL-4, IL-6, TNF-alpha, IL-10 and IL-12 were higher in the sera of MRL/lpr mice. The FO diet lowered the levels of these cytokines (except IL-4) and lipid mediators. Adding 500 IU of vit-E to the FO diet further lowered the levels of IL-6, IL-10, IL-12, and TNF-alpha. CONCLUSION: It is clear from our observations that the beneficial effects of FO can be enhanced by the addition of 500 IU of vit-E in the diet. The FO diet containing 500 IU of vit-E may specifically modulate the levels of IL-6, IL-10, IL-12 and TNF-alpha and thereby may delay the onset of autoimmunity in the MRL/lpr mouse model. The observations from this study may form a basis for selective nutrition intervention based on specific fatty acids and antioxidants in delaying the progress of RA.

Animals↗
PubMed1967

The formation and properties of thin lipid membranes from HK and LK sheep red cell lipids.

Lipids were obtained from high potassium (HK) and low potassium (LK) sheep red cells by sequential extraction of the erythrocytes with isopropanol-chloroform, chloroform-methanol-0.1 M KCl, and chloroform. The extract contained cholesterol and phospholipid in a molar ratio of 0.8:1.0, and less than 1% protein contaminant. Stable thin lipid membranes separating two aqueous compartments were formed from an erythrocyte lipid-hydrocarbon solution, and had an electrical resistance of approximately 10(8) ohm-cm(2) and a capacitance of 0.38-0.4 microf/cm(2). From the capacitance values, membrane thickness was estimated to be 46-132 A, depending on the assumed value for the dielectric constant (2.0-4.5). Membrane voltage was recorded in the presence of ionic (NaCl and/or KCl) concentration gradients in the solutions bathing the membrane. The permeability of the membrane to Na(+), K(+), and Cl(-) (expressed as the transference number, T(ion)) was computed from the steady-state membrane voltage and the activity ratio of the ions in the compartments bathing the membrane. T(Na) and T(K) were approximately equal ( approximately 0.8) and considerably greater than T(Cl) ( approximately 0.2). The ionic transference numbers were independent of temperature, the hydrocarbon solvent, the osmolarity of the solutions bathing the membranes, and the cholesterol content of the membranes, over the range 21-38 degrees C. The high degree of membrane cation selectivity was tentatively attributed to the negatively charged phospholipids (phosphatidylethanolamine and phosphatidylserine) present in the lipid extract.

Animals↗
PubMed2003

Dynamic and regulated association of caveolin with lipid bodies: modulation of lipid body motility and function by a dominant negative mutant.

Caveolins are a crucial component of caveolae but have also been localized to the Golgi complex, and, under some experimental conditions, to lipid bodies (LBs). The physiological relevance and dynamics of LB association remain unclear. We now show that endogenous caveolin-1 and caveolin-2 redistribute to LBs in lipid loaded A431 and FRT cells. Association with LBs is regulated and reversible; removal of fatty acids causes caveolin to rapidly leave the lipid body. We also show by subcellular fractionation, light and electron microscopy that during the first hours of liver regeneration, caveolins show a dramatic redistribution from the cell surface to the newly formed LBs. At later stages of the regeneration process (when LBs are still abundant), the levels of caveolins in LBs decrease dramatically. As a model system to study association of caveolins with LBs we have used brefeldin A (BFA). BFA causes rapid redistribution of endogenous caveolins to LBs and this association was reversed upon BFA washout. Finally, we have used a dominant negative LB-associated caveolin mutant (cavDGV) to study LB formation and to examine its effect on LB function. We now show that the cavDGV mutant inhibits microtubule-dependent LB motility and blocks the reversal of lipid accumulation in LBs.

Animals↗
PubMed2006

Lipid phosphate phosphatases 1 and 3 are localized in distinct lipid rafts.

Lipid phosphate phosphatases (LPPs), integral membrane proteins with six transmembrane domains, dephosphorylate a variety of extracellular lipid phosphates. Although LPP3 is already known to bind to Triton X-100-insoluble rafts, we here report that LPP1 is also associated with lipid rafts distinct from those harboring LPP3. We found that LPP1 was Triton X-100-soluble, but CHAPS-insoluble in LNCaP cells endogenously expressing LPP1 and several LPP1 cDNA-transfected cells including NIH3T3 fibroblasts. In addition to the non-ionic detergent insolubility, LPP1 further possessed several properties formulated for raft-localizing proteins as follows: first, the CHAPS-insolubility was resistant to the actin-disrupting drug cytochalasin D; second, the CHAPS-insoluble LPP1 floated in an Optiprep density gradient; third, the CHAPS insolubility of LPP1 was lost by cholesterol depletion; and finally, the subcellular distribution pattern of LPP1 exclusively overlapped with that of a raft marker, cholera toxin B subunit. Interestingly, confocal microscopic analysis showed that LPP1 was distributed to membrane compartments distinct from those of LPP3. Analysis using various LPP1/LPP3 chimeras revealed that their first extracellular regions determine the different Triton X-100 solubilities. These results indicate that LPP1 and LPP3 are distributed in distinct lipid rafts that may provide unique microenvironments defining their non-redundant physiological functions.

Animals↗
PubMed2000

Conjugated linoleic acids exhibit a strong fat-to-lean partitioning effect, reduce serum VLDL lipids and redistribute tissue lipids in food-restricted rats.

Effects of conjugated linoleic acids (CLA) on a series of metabolic events are expected to depend on the feeding regimen and levels of energy ingested. This study was the first examining the mode of action of CLA on body composition, tissue lipids, lipoproteins and hepatic enzymes in situations of enhanced fat store mobilization. Two groups of male growing Sprague-Dawley rats were fed for 3 wk a diet containing 0 (control group) or 3 g/100 g of a CLA mixture at the expense of sunflower oil, and were then subjected to a weight-loss feeding regimen for another 18 d. Rats fed the CLA-fortified diet gained 11% less weight than the control rats (P<0.05). Rats fed the high CLA diet had less body fat (1.47+/-0.16 vs. 1.07+/-0.09 g/100g, P<0.05) and a higher lean deposition (25.6+/-0.2 vs. 28.4+/-0.3 g/100 g, P<0.05) than control rats. CLA-fed rats had a 41% lower cholesterol concentration in liver than the control rats (P<0.05). Some differences in glycerophospholipid subclass profile of liver and erythrocyte membrane were observed; the hepatic concentrations of phosphatidylethanolamine (4.76+/-0.46 vs. 6.86+/-0.99 micromol/g, P = 0.07) and phosphatidylcholine (12.9+/-0.5 vs. 15.3+/-1.2 micromol/g, P = 0.09) tended to be greater and the level of phosphatidylcholine in erythrocyte membranes was significantly greater (1.40+/-0.12 vs. 1.83 +/-0.16 micromol/g, P<0.05) in the CLA-treated group than in the control group. The activities of catalase and ornithine decarboxylase in liver did not differ between the groups. Further, CLA-treated rats had significantly lower serum concentrations of VLDL lipids than control rats, whereas concentrations of LDL and HDL lipids were unaffected. The results indicate that a high dose of a CLA mixture is a strong repartitioning agent and a modulator of lipid metabolism under conditions of enhanced fat store mobilization in rats.

Adipose Tissue↗
PubMed1996

Gender-based mortality follow-up from the Program on the Surgical Control of the Hyperlipidemias (POSCH) and meta-analysis of lipid intervention trials. Women in POSCH and other lipid trials.

OBJECTIVE: The authors assessed the clinical results of lipid-lowering therapy in women. SUMMARY BACKGROUND DATA: The Program on the Surgical Control of the Hyperlipidemias (POSCH) has demonstrated that effective lowering of total cholesterol and low-density lipoprotein cholesterol in a postmyocardial infarction population significantly reduces atherosclerotic coronary heart disease (ACHD) mortality, ACHD mortality combined with a new confirmed nonfatal myocardial infarction, and the number of coronary artery bypass grafting and angioplasty procedures performed. METHODS: A review and meta-analysis were performed of the seven primary or secondary lipid/ atherosclerosis intervention trials-including POSCH-published in the English-language literature that included women and published results in women separate from the results in men or in the entire trial population. The main outcome measure analyzed was overall mortality. RESULTS: The Scottish Physicians Clofibrate Study, the Newcastle upon Tyne Clofibrate Study, and the Pravastatin Limitation of Atherosclerosis in the Coronary Arteries (PLAC I) Trial may have demonstrated a possible benefit in ACHD prognosis from effective lipid intervention in women. The other four available trials did not. The Minnesota Coronary Survey reported a 15.6% increase in overall mortality rate and a 30.6% increase in a combined cardiovascular endpoint rate in the lipid-intervention group. The Upjohn Colestipol Study demonstrated statistically significant reductions in overall and ACHD mortality in the men, but not in the women. The Scandinavian.

Cholesterol↗
PubMed1970

Effect of Growth Temperature on the Lipid Composition of Cyanidium caldarium: I. Class Separation of Lipids.

Cyanidium caldarium was cultured at 20 and 55 C and harvested during exponential growth phase. Comparative lipid studies on each cell type show a decrease by one-half of the total lipid in cells grown at 55 C over cells grown at 20 C. While the distribution of lipid into each of five lipid classes was not influenced by high temperature (55 C), the degree of unsaturation was greatly affected. Ratios of unsaturated to saturated fatty acids in these cells decreased 3-fold with increased temperature in the growth environment. Cells cultured at 20 C contained 30% of their fatty acids as linolenic while this fatty acid could not be detected in cells cultured at 55 C.

Journal Article↗
PubMed1980

Lipid-protein interactions in human erythrocyte-membrane acetylcholinesterase. Modulation of enzyme activity by lipids.

Purified human erythrocyte membrane acetylcholinesterase was incorporated into vesicles of various lipid compositions. The activities of the free and the lipid-associated enzyme were assayed at temperatures between 4 degrees C and 40 degrees C and the results were visualized as plots of log v versus 1/T (Arrhenius plots). For the purified, detergent-depleted enzyme a linear relation was obtained. If Triton X-100 was added to the assay medium a curved plot resulted. For acetylcholinesterase incorporated into dimyristoylphosphatidylcholine vesicles a clear break in the plot was observed at the phase transition temperature of the lipid. With lipids not experiencing a phase transition within the temperature range investigated, again a linear relation was obtained. These results show that the activity of human erythrocyte membrane acetylcholinesterase is strongly modulated by its hydrophobic environment.

Acetylcholinesterase↗
PubMed1976

Lipid composition and lipid metabolism of Spiroplasma citri.

In a horse serum-based medium containing a full complement of fatty acids, cells of Spiroplasma citri were seen to preferentially incorporate palmitic acid. In the same medium, which had a steryl ester-to-sterol ratio of 3.64, a steryl ester-to-sterol ratio of 0.23 was seen in the cells, cholesterol being preferentially incorporated over cholesteryl ester. Like most other mycoplasmas, S. citri was shown to be unable to synthesize fatty acids or esterify cholesterol. The neutral lipids of S. citri grown in a medium containing horse serum consisted of free cholesterol, cholesteryl ester, free fatty acids, triglycerides and diglycerides. All polar lipids were phospholipids, with no glycolipids detected. These phospholipids, which are characteristic of many mycoplasmas, are phosphatidyl glycerol, diphosphatidyl glycerol, and their lyso derivatives. Sphingomyelin was also incorporated when cells were grown on horse serum. A sterol requirement for the growth of S. citri was confirmed using a serum-free medium supplemented with bovine serum albumin, palmitic acid, and various concentrations of sterols dissolved in Tween 80. The addition of palmitic acid stimulated growth but was not essential for growth. S citri was shown to grow best on cholesterol and beta-sitosterol and was able to grow on stigmasterol and ergosterol to a lesser degree. No growth was obtained using mevalonate, deoxycholate, or taurodeoxycholate as an alternative to sterol. S. citri was also able to grow when palmitic acid was replaced with oleic acid, linoleic acid, or linolenic acid. Alterations in the lipid composition of the growth medium and hence in the lipid composition of S. citri induced changes in the characteristic helical morphology of the cells, concurrent with loss of cell viability. Culture, age, and pH were also factors in determining cell morphology and viability.

Cholesterol↗
PubMed1999

Lipid transfer inhibitor protein defines the participation of lipoproteins in lipid transfer reactions: CETP has no preference for cholesteryl esters in HDL versus LDL.

Cholesteryl ester transfer protein (CETP) catalyzes the net transfer of cholesteryl ester (CE) between lipoproteins in exchange for triglyceride (heteroexchange). It is generally held that CETP primarily associates with HDL and preferentially transfers lipids from this lipoprotein fraction. This is illustrated in normal plasma where HDL is the primary donor of the CE transferred to VLDL by CETP. However, in plasma deficient in lipid transfer inhibitor protein (LTIP) activity, HDL and LDL are equivalent donors of CE to VLDL (Arterioscler Thromb Vasc Biol. 1997;17:1716-1724). Thus, we have hypothesized that the preferential transfer of CE from HDL in normal plasma is a consequence of LTIP activity and not caused by a preferential CETP-HDL interaction. We have tested this hypothesis in lipid mass transfer assays with partially purified CETP and LTIP, and isolated lipoproteins. With a physiological mixture of lipoproteins, the preference ratio (PR, ratio of CE mass transferred from a lipoprotein to VLDL versus its CE content) for HDL and LDL in the presence of CETP alone was approximately 1 (ie, no preference). Fourfold variations in the LDL/HDL ratio or in the levels of HDL in the assay did not result in significant preferential transfer from any lipoprotein. On addition of LTIP, the PR for HDL was increased up to 2-fold and that for LDL decreased in a concentration-dependent manner. Under all conditions where LDL and HDL levels were varied, LTIP consistently resulted in a PR >1 for CE transfer from HDL. Short-term experiments with radiolabeled lipoproteins and either partially purified or homogenous CETP confirmed these observations and further demonstrated that CETP has a strong predilection to mediate homoexchange (bidirectional transfer of the same lipid) rather than heteroexchange (CE for TG); LTIP had no effect on the selection of CE or TG by CETP or its mechanism of action. We conclude, in contrast to current opinion, that CETP has no preference for CE in HDL versus LDL, suggesting that the previously reported stable binding of CETP to HDL does not result in selective transfer from this lipoprotein. These data suggest that LTIP is responsible for the preferential transfer of CE from HDL that occurs in plasma. CETP and LTIP cooperatively determine the extent of CETP-mediated remodeling of individual lipoprotein fractions.

Apolipoproteins↗
PubMed2000

Direct visualization of lipid deposition and reverse lipid transport in a perfused artery : roles of VLDL and HDL.

The major goal of this study was to determine the interactions of VLDL surface and core lipids with the artery wall. We first demonstrated in vitro that surface lipid in VLDL could be traced using the phospholipid-like fluorescent probe 1,1'-dioctadecyl-3,3, 3',3'-tetramethyl-indocarbocyanine (DiI). The core of VLDL particles was traced by fluorescently labeling apolipoprotein B with TRITC. The labeled VLDLs were perfused through rat carotid arteries, and accumulation of the fluorescently labeled VLDL components in the arterial walls was determined by quantitative fluorescence microscopy. Addition of lipoprotein lipase increased the accumulation of both DiI and TRITC by >2.3-fold. Histological examination showed that DiI and TRITC were primarily localized to the endothelial layer; however, DiI also accumulated as small "lakes" deeper in the artery, in a subendothelial position. Addition of HDL to the perfusion decreased the accumulation of surface lipid and apolipoprotein B-containing particles and eliminated the DiI lakes. Moreover, the increase in endothelial layer permeability associated with lipolysis was attenuated 21% by HDL. If VLDL surface lipid first was allowed to accumulate in the arterial wall, its subsequent rate of loss was more than twice as fast if HDL was included in the perfusate. These studies directly demonstrate atherogenic effects of VLDL lipolysis and their inhibition by HDL.

Animals↗