scholarly journals Small high density lipoprotein subclasses: some of their physico-chemical properties and stability in solution.

2005 ◽  
Vol 52 (2) ◽  
pp. 515-525 ◽  
Author(s):  
Ragheb F Atmeh ◽  
Issa O Abd Elrazeq
Keyword(s):  
Surface Charge ◽  
Diffusion Coefficients ◽  
Electrical Potential ◽  
Chemical Properties ◽  
Density Lipoprotein ◽  
Polyacrylamide Gel ◽  
High Density ◽  
High Density Lipoproteins ◽  
Physico Chemical ◽  
And Diffusion

Small high density lipoproteins (SHDL) contribute to the protection from atherosclerosis, but detailed information about their properties is not available yet. We isolated four of the smallest HDL subclasses that contain apoA-I alone, the small lipoprotein A-I (SLpAI), by their separation on gradient polyacrylamide gel followed by electroelution. Their physico-chemical properties were calculated from their displacement in non-denaturing gradient polyacrylamide gel under the effect of electrical potential. The properties are: Stokes' radii 2.96-3.56 nm; molecular masses 42-70 kDa; net negative charge 7.2-13.5; surface charge densities 3139-4069 -esu.cm(-2); surface potentials 10.6-15.7 -mV; coefficients of friction 5.74-6.90 x 10(-8) g.s(-1); and diffusion coefficients 5.76-6.94 x 10(-7) cm(2).s(-1). We found that these particles were of low stability as they underwent molecular transformation into larger particles on storage. The estimated dimensions of these particles do not support ellipsoidal shape, therefore, the most probable shape is spherical; consequently, their hydrated characteristics were estimated. We conclude that these particles have high values of negative surface charge and diffusion coefficients, and are of low stability. Their small Stokes' radii were similar to each other and they are spherical and highly hydrated.

Changes in chemical composition and physico-chemical properties of chick low- and high-density lipoproteins induced by supplementation of coconut oil to the diet

Biochimie ◽  
1997 ◽  
Vol 79 (6) ◽  
pp. 333-340 ◽  
Author(s):  
E.M. Talavera ◽  
M.F. Zafra ◽  
A. Gil-Villarino ◽  
M.I. Pérez ◽  
J.M. Alvarez-Pez ◽  
...  
Keyword(s):  
Chemical Composition ◽  
Chemical Properties ◽  
Coconut Oil ◽  
High Density ◽  
High Density Lipoproteins ◽  
Physico Chemical

scholarly journals Branched Synthetic Constructs that Mimic the Physico-Chemical Properties of Apolipoprotein AI in Reconstituted High-Density Lipoproteins

1996 ◽  
Vol 239 (1) ◽  
pp. 74-84 ◽  
Author(s):  
Ludovic Demoor ◽  
Christophe Boutillon ◽  
Catherine Fievet ◽  
Berlinda Vanloo ◽  
Johan Baert ◽  
...  
Keyword(s):  
Chemical Properties ◽  
High Density ◽  
High Density Lipoproteins ◽  
Apolipoprotein Ai ◽  
Physico Chemical

Effect of homocysteinylation on high density lipoprotein physico-chemical properties

2010 ◽  
Vol 163 (2) ◽  
pp. 228-235 ◽  
Author(s):  
Gianna Ferretti ◽  
Tiziana Bacchetti ◽  
Simona Masciangelo ◽  
Virginia Bicchiega
Keyword(s):  
High Density Lipoprotein ◽  
Chemical Properties ◽  
Density Lipoprotein ◽  
High Density ◽  
Physico Chemical

scholarly journals High-Density Lipoproteins and Cardiovascular Disease: The Good, the Bad and the Future

Biomedicines ◽  
2021 ◽  
Vol 9 (8) ◽  
pp. 857
Author(s):  
Josep Julve ◽  
Joan Carles Escolà-Gil
Keyword(s):  
Cardiovascular Disease ◽  
High Density Lipoprotein ◽  
High Density Lipoprotein Cholesterol ◽  
Density Lipoprotein ◽  
Epidemiological Studies ◽  
High Density ◽  
High Density Lipoproteins ◽  
Atherosclerotic Cardiovascular Disease ◽  
Plasma High Density ◽  
Low Levels

Epidemiological studies have shown that low levels of plasma high-density lipoprotein cholesterol (HDL-C) are associated with increased atherosclerotic cardiovascular disease (CVD) [...]

scholarly journals High-Density Lipoproteins and the Kidney

Cells ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 764
Author(s):  
Arianna Strazzella ◽  
Alice Ossoli ◽  
Laura Calabresi
Keyword(s):  
Kidney Disease ◽  
Renal Disease ◽  
Cholesterol Acyltransferase ◽  
Density Lipoprotein ◽  
Hdl Cholesterol ◽  
High Density ◽  
High Density Lipoproteins ◽  
Lcat Deficiency ◽  
Progression Of Renal Disease ◽  
The Impact

Dyslipidemia is a typical trait of patients with chronic kidney disease (CKD) and it is typically characterized by reduced high-density lipoprotein (HDL)-cholesterol(c) levels. The low HDL-c concentration is the only lipid alteration associated with the progression of renal disease in mild-to-moderate CKD patients. Plasma HDL levels are not only reduced but also characterized by alterations in composition and structure, which are responsible for the loss of atheroprotective functions, like the ability to promote cholesterol efflux from peripheral cells and antioxidant and anti-inflammatory proprieties. The interconnection between HDL and renal function is confirmed by the fact that genetic HDL defects can lead to kidney disease; in fact, mutations in apoA-I, apoE, apoL, and lecithin–cholesterol acyltransferase (LCAT) are associated with the development of renal damage. Genetic LCAT deficiency is the most emblematic case and represents a unique tool to evaluate the impact of alterations in the HDL system on the progression of renal disease. Lipid abnormalities detected in LCAT-deficient carriers mirror the ones observed in CKD patients, which indeed present an acquired LCAT deficiency. In this context, circulating LCAT levels predict CKD progression in individuals at early stages of renal dysfunction and in the general population. This review summarizes the main alterations of HDL in CKD, focusing on the latest update of acquired and genetic LCAT defects associated with the progression of renal disease.

Abstract 260: Knockout of Apolipoprotein A-II Has Dramatic Effects on High-Density Lipoprotein Subspecies Distribution

2012 ◽  
Vol 32 (suppl_1) ◽  
Author(s):  
Scott M Gordon ◽  
Catherine A Reardon ◽  
Godfrey S Getz ◽  
W S Davidson
Keyword(s):  
Gel Filtration ◽  
Density Lipoprotein ◽  
High Density ◽  
Paraoxonase 1 ◽  
High Density Lipoproteins ◽  
Ionization Mass ◽  
Associated Proteins ◽  
Compositional Diversity ◽  
The Impact ◽  
Modest Effect

High density lipoproteins (HDL) are a highly heterogeneous population of particles composed of various lipids and proteins. They have been demonstrated to possess a diverse variety of functional properties which are thought to contribute to protection against cardiovascular disease (CVD). Proteomics studies have identified up to 75 different proteins which can associate with HDL. The basis for the compositional diversity of HDL is not known but a better understanding will yield important information about its broad functional diversity. To investigate the impact of common HDL apolipoproteins on the distribution of other apolipoproteins, we have begun to systematically fractionate plasma from various HDL apolipoprotein KO mice. Plasma from apoA-I, apoA-IV and apoA-II global KO mice was applied to gel filtration chromatography to distinguish HDL size populations. HDL particles sequestered by a phospholipid binding resin were proteomically analyzed by electrospray ionization mass spectrometry. By comparing elution volume shifts (i.e. particle size variations) for each HDL protein between WT controls and the KO models, we assessed the impact of the deleted protein on HDL size distributions. Ablation of apoA-I, while decreasing total HDL phospholipid by 70%, had a surprisingly small impact on the distribution of the majority of other HDL associated proteins - affecting only 9 of them. Genetic apoA-IV ablation had a similar modest effect shifting a distinct subset of 9 proteins. However, loss of apoA-II, in addition to causing a similar 70% reduction in overall HDL phospholipids, affected the size distribution of some 45 HDL proteins (including several complement proteins and paraoxonase-1). These data suggest that apoA-I, while associated with the majority of HDL phospholipid, may actually interact with relatively few of the lower abundance proteins known to be associated with HDL. ApoA-II on the other hand, may interact with many of these, perhaps acting as a docking site or adaptor molecule.

Involvement of high-density lipoprotein in stimulatory effect of hormones supporting function of the bovine corpus luteum.

2003 ◽  
Vol 51 (1) ◽  
pp. 111-120 ◽  
Author(s):  
D. Skarżyński ◽  
J. Młynarczuk ◽  
J. Kotwica
Keyword(s):  
Luteinising Hormone ◽  
Density Lipoprotein ◽  
High Density ◽  
High Density Lipoproteins ◽  
Luteal Cells ◽  
Progesterone Secretion ◽  
Bovine Corpus Luteum ◽  
Progesterone Synthesis ◽  
Deficient Medium ◽  
Intracellular Pathway

The hypothesis that epinephrine (noradrenaline, NA) enhances utilisation of high-density lipoproteins (HDL) by bovine luteal cells and that this process involves phospholipase (PL) C and protein kinase (PK) C intracellular pathway was tested. Luteal cells from days 2-4, 5-10 or 11-17 of the oestrous cycle were pre-incubated for 20h. Subsequently DMEM/Ham's F-12 medium was replaced by fresh medium and the cells were treated for 6 h as follows: In Experiment I with HDL (5-75μg cholesterol per ml), NA, isoprenaline (ISO) or luteinising hormone (LH). In Experiment II cells were incubated for further 24h in deficient medium (without FCS) and next treated as in Experiment I. In Experiment III cells were stimulated with NA, ISO or LH alone and together with HDL. In Experiment IV cells were treated with PLC inhibitor (U-73122) or with PKC inhibitor (staurosporine) or stimulator (phorbol 12-myristrate 13-acetate) and with either NA, insulin or LH. Only luteal cells from days 5-10 of the cycle responded on HDL and β-mimetics (P<0.05). LH stimulated progesterone secretion from the luteal cells during all stages of the cycle (P<0.001). Cells incubated in deficient medium and supplemented with HDL secreted as much progesterone as those stimulated by LH in all stages of the cycle. Beta-mimetics were unable to enhance the stimulatory effect of HDL. Blockade of PLC had no influence on progesterone secretion from cells treated with either NA or LH, but this did impair the stimulatory effect of insulin (P<0.05). Similarly, blockade of PKC by staurosporine impaired (P<0.05) the effect of insulin only but not that observed after LH or NA treatment. We suggest that: (a) noradrenergic stimulation does not enhance utilisation of cholesterol from HDL for progesterone secretion; (b) the fasting of luteal cells seems to activate enzymes responsible for the progesterone synthesis; (c) effect of NA on progesterone secretion from luteal cells does not involve the PLC-PKC pathway.

Abstract 617: Intestine-Specific MTP Deficiency with ACAT2 Gene Ablation Lowers Acute Cholesterol Absorption With Chylomicrons and High-Density Lipoproteins

2014 ◽  
Vol 34 (suppl_1) ◽  
Author(s):  
Jahangir Iqbal ◽  
Mohamed Boutjdir ◽  
Lawrence L Rudel ◽  
M Mahmood Hussain
Keyword(s):  
Density Lipoprotein ◽  
Microsomal Triglyceride Transfer Protein ◽  
Cholesterol Absorption ◽  
High Density ◽  
High Density Lipoproteins ◽  
High Cholesterol ◽  
Intestinal Cholesterol Absorption ◽  
Triglyceride Accumulation ◽  
Abca1 Expression ◽  
Deficient Mice

Intestinal cholesterol absorption involves chylomicron and high density lipoprotein (HDL) pathways. Microsomal triglyceride transfer protein (MTP) and ATP binding cassette family A protein 1 (ABCA1) are critical for cholesterol transport by these pathways, respectively. Additionally, acyl Co-A:cholesterol acyltransferase 2 (ACAT2) plays an important role in cholesterol absorption. Intestinal MTP ablation significantly increased intestinal triglyceride and cholesterol levels and reduced their acute absorption. In contrast, ACAT2 deficiency had no effect on triglyceride absorption but significantly reduced cholesterol absorption. Individual deficiencies of ACAT2 and MTP reduced cholesterol absorption with chylomicrons. We hypothesized that their combined deficiency would increase cholesterol secretion with HDL; unexpectedly, their deficiency reduced secretion with both chylomicrons and HDL. Further, we observed significant reductions in intestinal ABCA1 expression in combined deficient mice. Thus, free cholesterol is unavailable for secretion by the HDL pathway in these mice. We speculate that reductions in ABCA1 expression and HDL secretion might be secondary to massive triglyceride accumulation associated with intestinal MTP deficiency. Besides its role in cholesterol absorption, ACAT2 deficiency causes mild hypertriglyceridemia and reduces steatosis in mice fed high cholesterol diets by increasing hepatic lipoprotein production by unknown mechanisms. We show that this phenotype is preserved in the absence of intestinal MTP in ACAT2 deficient mice fed a Western diet. Further, we observed increases in hepatic MTP activity in these mice. Thus, ACAT2 deficiency might increase MTP expression to avoid steatosis. Therefore, ACAT2 inhibition might avert steatosis associated with high cholesterol diets by increasing MTP expression.

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