Search results for "LIPOPROTEINS"
showing 10 items of 495 documents
Modified lipoproteins as contrast agents for imaging of atherosclerosis.
2007
The ability to detect and characterize atherosclerosis with targeted contrast agents may enable initiation of therapy for atherosclerotic lesions prior to becoming symptomatic. Since lipoproteins such as high-density lipoprotein (HDL) and low-density lipoprotein (LDL) play a critical role in the regulation of plaque biology through the transport of lipids into and out of atherosclerotic lesions, modifying HDL and LDL with radioisotopes for nuclear imaging, chelates for magnetic resonance imaging (MRI) or other possible contrast agents for computed tomography imaging techniques may aid in the detection and characterization of atherosclerosis. This review focuses on the literature employing l…
Periodontitis, blood lipids and lipoproteins
2014
Periodontitis, one of the most common chronic infections in adults, is characterized by the accumulation of dental plaque and infection by gram-negative pathogens bacteria, which further lead to the destruction of periodontal tissues. A relationship between chronic periodontitis and abnormalities in lipid and/or lipoprotein metabolism is not well understood yet. Periodontitis is associated with elevated pro-atherogenic plasma-lipids, including small dense LDL, while oxidized LDL may act as inflammatory stimulant in periodontitis. Periodontal pathogens may directly modify lipoprotein, including protective characteristics of HDL and contribute to development of metabolic syndrome, Type 2 diab…
The Pandinus imperator haemolymph lipoprotein, an unusual phosphatidylserine carrying lipoprotein.
2009
The haemolymph lipoprotein of the scorpion, Pandinus imperator was isolated and characterised. Contrary to the lipoproteins of insects and the discoidal HDL-lipoproteins of a crayfish and polychaete, the Pandinus lipoprotein consists of three instead of two apoproteins (apoPiLp I = 230 kDa, apoPiLp II = 130 kDa and apoPiLp III = 120 kDa). The apolipoproteins are arranged in varying stoichiometries as judged by cross-linking experiments. In lipoprotein samples from individual animals, the two smaller subunits occurred in a 1:1 stoichiometry, while the relative amount of the 230 kDa peptide varied. The lipoprotein is a slightly heart-shaped HDL with a diameter of approximately 15 nm. It is pr…
Lecithin-cholesterol-acyltransferase deficiency: autosomal recessive transmission in a large kindred.
2008
Thirty-four members of a single Sardinian kindred with lecithin-cholesterol-acyltransferase deficiency have been studied. The kindred spans four generations and the parents of the two affected siblings are blood relatives. Segregation of the acyltransferase deficiency gene in the family clearly demonstrated an autosomal recessive mode of inheritance. Thirteen family members, including all obligate heterozygotes, had roughly half-normal acyltransferase activities (mean +/- S.D. = 0.39 +/- 0.06 mU/ml) when compared to 17 intrafamilial controls and spouses (mean +/- S.D. = 0.72 +/- 0.09 mU/ml) and 40 blood donors from Marburg/Lahn (mean +/- S.D. =0.76 +/- 0.1 mU/ml). Characterization of the he…
Lipoprotein profile and high-density lipoproteins: subfractions distribution in centenarians.
1998
In order to assess the role of HDL on longevity, we studied HDL subfraction distribution in centenarian women compared with a group of weight- and gender-matched healthy normolipidemic controls. We did not find any significant difference in the mean plasma lipid, apolipoprotein, and Lp(a) levels. On the contrary, in spite of similar HDL-cholesterol concentrations (1.32 ± 0.41 mmol/l in centenarians vs. 1.32 ± 0.25 mmol/l in controls, p = not significant), HDL<sub>2b</sub> and HDL<sub>3a</sub> levels were, respectively, significantly increased and significantly reduced in centenarians in comparison with controls (HDL<sub>2b</sub> 32.4 ± 9.2% in centenarian…
Possible protective role for C-reactive protein in atherogenesis: complement activation by modified lipoproteins halts before detrimental terminal se…
2004
Background—Previous work indicated that enzymatically remodeled LDL (E-LDL) might activate complement in atherosclerotic lesions via a C-reactive protein (CRP)–dependent and CRP-independent pathway. We sought to substantiate this contention and determine whether both pathways drive the sequence to completion.Methods and Results—E-LDL was prepared by sequential treatment of LDL with a protease and cholesteryl esterase. Trypsin, proteinase K, cathepsin H, or plasmin was used with similar results. Functional tests were used to assess total complement hemolytic activity, and immunoassays were used to demonstrate C3 cleavage and to quantify C3a, C4a, C5a, and C5b-9. E-LDL preparations activated …
Genetic diagnosis of familial hypercholesterolemia in a South European outbreed population: influence of low-density lipoprotein (LDL) receptor gene …
2001
The aims of this study were to examine the presence of mutations in the low-density lipoprotein receptor gene among subjects clinically diagnosed with familial hypercholesterolemia and to analyze whether the molecular diagnosis helps to predict the response to simvastatin treatment in our familial hypercholesterolemia population. Fifty-five probands and 128 related subjects with familial hypercholesterolemia were studied. Genetic diagnosis was carried out following a three-step protocol based on Southern blot and PCR-single strand conformational polymorphism analysis. A randomized clinical trial with simvastatin was conducted in 42 genetically diagnosed subjects with familial hypercholester…
Italian familial defective apolipoprotein B patients share a unique haplotype with other Caucasian patients.
2001
Familial defective apolipoprotein (apo) B-100 together with familial hypercholesterolemia are the two common genetic conditions that cause hypercholesterolemia. Familial defective apolipoprotein B-100 is due to mutations around codon 3500 of the apo B gene. The most-characterized mutation is a G>A transition at nucleotide 10,708 that results in the substitution of arginine by glutamine at codon 3500 (Apo B Arg3500Gln). Two other mutations are caused by a C>T transition, one at nucleotide 10,800 (Apo B Arg3531Cys) and the other at nucleotide 10,707 (apo B Arg3500Trp). In the present study we describe three new Italian cases of familial defective apolipoprotein B-100 (Apo B Arg3500Gln), one f…
Lack of phenotypic additive effect of familial defective apolipoprotein B3531 in familial hypercholesterolaemia.
2020
Familial defective apolipoprotein (apo) B (FDB) and familial hypercholesterolaemia (FH) are the two common genetic conditions that cause hypercholesterolaemia. R3531C mutation of the APOB gene is a rare cause of FDB. Individuals with both FDB and FH are rare. A 51-year-old man with hypercholesterolaemia (11.4 mmol/L) and his family were studied. Low-density lipoprotein (LDL) receptor (LDLR) and APOB genes were analysed by direct sequencing. LDL of four subjects were studied in a fibroblast LDL receptor-binding displacement assay. We found a mutation of the LDLR gene (p.Y398X) in the proband and in four other family members: the p.R3531C APOB gene mutation was also found in the proband, his …
Fatty acids liberated from low-density lipoprotein trigger endothelial apoptosis via mitogen-activated protein kinases.
2005
Enzymatic modification of low-density lipoprotein (LDL) as it probably occurs in the arterial intima drastically increases its cytotoxicity, which could be relevant for the progression of atherosclerotic lesions. LDL was treated with a protease and cholesterylesterase to generate a derivative similar to lesional LDL, with a high content of free cholesterol and fatty acids. Exposure of endothelial cells to the enzymatically modified lipoprotein (E-LDL), but not to native or oxidized LDL, resulted in programmed cell death. Apoptosis was triggered by apoptosis signal-regulating kinase 1 dependent phosphorylation of p38. Depletion and reconstitution experiments identified free fatty acids (FFA)…