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Hsp104 facilitates the endoplasmic-reticulum-associated degradation of disease-associated and aggregation-prone substrates.

Misfolded proteins in the endoplasmic reticulum (ER) are selected for ER-associated degradation (ERAD). More than 60 disease-associated proteins are substrates for the ERAD pathway due to the presence of missense or nonsense mutations. In yeast, the Hsp104 molecular chaperone disaggregates detergent-insoluble ERAD substrates, but the spectrum of disease-associated ERAD substrates that may be aggregation prone is unknown. To determine if Hsp104 recognizes aggregation-prone ERAD substrates associated with human diseases, we developed yeast expression systems for a hydrophobic lipid-binding protein, apolipoprotein B (ApoB), along with a chimeric protein harboring a nucleotide-binding domain from the cystic fibrosis transmembrane conductance regulator (CFTR) into which disease-causing mutations were introduced. We discovered that Hsp104 facilitates the degradation of ER-associated ApoB as well as a truncated CFTR chimera in which a premature stop codon corresponds to a disease-causing mutation. Chimeras containing a wild-type version of the CFTR domain or a different mutation were stable and thus Hsp104 independent. We also discovered that the detergent solubility of the unstable chimera was lower than the stable chimeras, and Hsp104 helped retrotranslocate the unstable chimera from the ER, consistent with disaggregase activity. To determine why the truncated chimera was unstable, we next performed molecular dynamics simulations and noted significant unraveling of the CFTR nucleotide-binding domain. Because human cells lack Hsp104, these data indicate that an alternate disaggregase or mechanism facilitates the removal of aggregation-prone, disease-causing ERAD substrates in their native environments.

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The non-enzymatic glycation of LDL proteins results in biochemical alterations - A correlation study of Apo B-AGE with obesity and rheumatoid arthritis.

Advanced glycation end-products (AGEs) can aggregate amid incessant inflammation, as may be available in patients with rheumatoid arthritis. d-Ribose reacts more promptly than glucose monosaccharide to the proteins and forms heterogeneous group of products known as AGEs. Obesity includes persons with provocative joint inflammation with increased lipid profile. Immunogenic evidences recommend a cross-sectional relationship between glycated LDL-Apo B100 and inflammation. The point of this examination was to look at the connection between d-ribose glycated ApoB100 (ApoB100-AGE) with obesity and rheumatoid arthritis. The binding specificity of auto-antibodies against ApoB100-AGE antigen present in obesity and rheumatoid arthritis patient's serum were inspected by direct binding and was further established by competitive inhibition ELISA. In the present study, hydroxyl radical, superoxide radical, ketoamine moieties, hydroxyl-methyl furfural (HMF) and carbonyl substances were evaluated in the patients' serum via respective specific methods. The prevalence of auto-antibodies against ApoB100-AGE antigen was recorded to be 58% and 52.86% from obese and rheumatoid arthritis patient respectively in contrast to its native analogue (P < 0.001). Moreover, the autoantibodies present in obese and arthritis patients were found to be highly specific towards ApoB100-AGE as confirmed by inhibition ELISA.

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Recent Advances in Fluorescent Angioscopy for Molecular Imaging of Human Atherosclerotic Coronary Plaque.

In vivo imaging of the native substances, including lipoproteins, that comprise human atherosclerotic plaques is currently beyond the scope of any available imaging techniques. Color and near-infrared fluorescent angioscopy (CFA and NIRFA, respectively) systems have been recently developed for molecular imaging of lipoproteins within the human coronary arterial wall ex vivo and/or in vivo. The author reviews recent findings on lipoprotein deposition in human coronary plaques obtained by these imaging techniques.

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Vaccination against T-cell epitopes of native ApoB100 reduces vascular inflammation and disease in a humanized mouse model of atherosclerosis.

The T-cell response to low-density lipoprotein (LDL) in the vessel wall plays a critical role in atherosclerotic plaque formation and stability. In this study, we used a new translational approach to investigate epitopes from human apolipoprotein B100 (ApoB100), the protein component of LDL, which triggers T-cell activation. We also evaluated the potential of two selected native ApoB100 epitopes to modulate atherosclerosis in human ApoB100-transgenic Ldlr (HuBL) mice.

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Ultrastructural organisation of HCV from the bloodstream of infected patients revealed by electron microscopy after specific immunocapture.

HCV particles are associated with very low-density lipoprotein components in chronically infected patients. These hybrid particles, or 'lipo-viro particles' (LVPs), are rich in triglycerides, and contain the viral RNA, the capsid protein, E1E2 envelope glycoproteins and apolipoproteins B and E. However, their specific ultrastructural organisation has yet to be determined. We developed a strategy for the preparation of any viral sample that preserves the native structure of the LVPs, facilitating their precise morphological characterisation.

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[Lipoprotein(a), its autoantibodies, and circulating T lymphocyte subpopulations as independent risk factors for coronary artery atherosclerosis].

To study the role of lipoprotein(a) [Lp(a)] as a potential autoantigen causing the activation of immunocompetent cells in atherosclerosis.

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Detection of Circulating Auto-Antibodies Against Ribosylated-LDL in Diabetes Patients.

This study analyzes effect of glycation on ApoB-100 residues by D-ribose as D-ribosylated-glycated LDL might be responsible for the cause of diabetes mellitus because of its far higher antigenic ability. The binding characteristics of circulating auto-antibodies in type 1 and type 2 diabetes patients against native and modified LDL were assessed.

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[The effect of increased concentration of lipoprotein (a) on identification of sub-faction of lipoproteins using native electrophoresis technique].

The quantitative analysis of sub-fractions of lipoproteins acquires growing significance in diagnostic and prognosis of cardiovascular diseases. It is well known that presence of lipoprotein (a) in high concentrations significantly distorts results of biochemical analysis, in particular detection of level of cholesterol of low-density lipoproteins. The lipoprotein (a) is a heterogeneous particle and its mobility in the systems used for analysis of sub-fractions of lipoproteins can have significant variability that will bring inaccuracy into results. The data concerning relationship between lipoprotein (a) and sub-fractions of lipoproteins and also their differentiation in various systems of determination of lipid spectrum are quite numerous. The given study is considered as actual one because it analyses input of lipoprotein (a) into results of detection of sub-fractions using the technique with diagnostic significance. The study was carried out for evaluating possible input of lipoprotein (a) into results of quantitative estimation of sub-fractions of lipoproteins by technique of native electrophoresis in polyacrylamide gel used for diagnostic of cardio-vascular diseases. To detect concentration of lipoprotein (a) in blood serum the technique of enzyme-linked immunosorbent assay was applied. The qualitative valuation of content of sub-fractions of lipoproteins was implemented using system Lipoprint Quantimetrix (USA). The sub-fractions of lipoproteins were detected in samples of serum of healthy donor and normolipidic patients before and after removal of lipoprotein (a) using technique of affine chromatography in vitro. It turned out that after removal of lipoprotein (a) analysis of sub-fractions of lipoproteins in plasma of healthy donor detects significant decreasing of level of lipoproteins of medium density. The samples of serum of patients with atherosclerosis besides removal of sub-fractions of lipoproteins of medium density, decreasing of level of large sub-fractions of low density lipoproteins was observed. The analysis of samples obtained after procedures of therapeutic lipoprotein (a) apheresis using columns “Lp (a) Lipopak” (Russia) demonstrated that along with removal of lipoprotein (a), decreasing of concentration of sub-fraction C lipoproteins of medium density in all samples that substantiates in vitro data. In patients without affection and with multi-vessel lesion of coronary bloodstream reliable differences in concentration of lipoproteins of medium density were established. The received data testify that high level of lipoprotein (a) can contribute significant inaccuracies into results of detection of subfractions of lipoproteins. Therefore, application of system Lipoprint (Quantimetrix USA) provides no opportunity to unequivocally interpret data concerning input of sub-fractions of lipoproteins into risk of development of cardio-vascular diseases in patients with pathological lipid profile and higher concentration of lipoprotein (a).

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Liver disease alters high-density lipoprotein composition, metabolism and function.

High-density lipoproteins (HDL) are important endogenous inhibitors of inflammatory responses. Functional impairment of HDL might contribute to the excess mortality experienced by patients with liver disease, but the effect of cirrhosis on HDL metabolism and function remain elusive. To get an integrated measure of HDL quantity and quality, we assessed several metrics of HDL function using apolipoprotein (apo) B-depleted sera from patients with compensated cirrhosis, patients with acutely decompensated cirrhosis and healthy controls. We observed that sera of cirrhotic patients showed reduced levels of HDL-cholesterol and profoundly suppressed activities of several enzymes involved in HDL maturation and metabolism. Native gel electrophoresis analyses revealed that cirrhotic serum HDL shifts towards the larger HDL2 subclass. Proteomic assessment of isolated HDL identified several proteins, including apoA-I, apoC-III, apoE, paraoxonase 1 and acute phase serum amyloid A to be significantly altered in cirrhotic patients. With regard to function, these alterations in levels, composition and structure of HDL were strongly associated with metrics of function of apoB-depleted sera, including cholesterol efflux capability, paraoxonase activity, the ability to inhibit monocyte production of cytokines and endothelial regenerative activities. Of particular interest, cholesterol efflux capacity appeared to be strongly associated with liver disease mortality. Our findings may be clinically relevant and improve our ability to monitor cirrhotic patients at high risk.

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Apolipoprotein B-100 Antibody Interaction With Atherosclerotic Plaque Inflammation and Repair Processes.

Treatment with IgG against the malondialdehyde (MDA)-modified apolipoprotein B-100 epitope p45 reduces atherosclerosis in experimental models. This study investigated the association between p45 IgG autoantibodies and plaque inflammation in subjects with advanced cardiovascular disease.

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