scholarly journals Inhibition of lymphocyte proliferation stimulated by lectins and allogeneic cells by normal plasma lipoproteins.

1977 ◽  
Vol 146 (6) ◽  
pp. 1791-1803 ◽  
Author(s):  
J H Morse ◽  
L D Witte ◽  
D S Goodman
Keyword(s):  
Human Plasma ◽  
Rank Order ◽  
Human Lymphocytes ◽  
Low Density Lipoproteins ◽  
Plasma Lipoproteins ◽  
High Density Lipoproteins ◽  
Low Density ◽  
Very Low Density Lipoproteins ◽  
Normal Plasma

Lipoproteins, isolated by sequential flotation at densities 1.006, 1.019, 1.063, and 1.21, were examined for their ability to inhibit human lymphocytes stimulated by allogeneic cells and by lectins (phytohemagglutinin-P and concanavalin A). All the classes of normal plasma lipoproteins inhibited lymphoproliferation when peripheral blood lymphocytes were cultured in autologous, heterologous, or lipoprotein-deficient plasma (d greater than 1.21). The rank order of inhibitory potency was intermediate density lipoprotein (IDL) greater than very low density lipoproteins (VLDL) greater than low density lipoproteins (LDL) greater than high density lipoproteins (HDL), regardless of the mode of stimulation. The concentrations of IDL, VLDL, and LDL required for complete inhibition of stimulated lymphoproliferation were considerably below the levels of each of these lipoproteins normally found in human plasma. In addition, the concentration of HDL required for 50-90% inhibition was in the range of HDL levels normally found in human plasma. Moreover, at relatively higher concentrations, lipoproteins suppressed the incorporation of [3H]thymidine into DNA below the levels seen with reseting, unstimulated lymphocytes. The results suggest that circulating lymphocytes may normally be highly suppressed by the combined effects of all the endogenous lipoproteins and that the lipoproteins may play important roles in vivo in modulating lymphocyte functions and responses.

scholarly journals Characterization of plasma lipoproteins separated and purified by agarose-column chromatography

1974 ◽  
Vol 139 (1) ◽  
pp. 89-95 ◽  
Author(s):  
Lawrence L. Rudel ◽  
Jason A. Lee ◽  
Manford D. Morris ◽  
James M. Felts
Keyword(s):  
Human Plasma ◽  
Column Chromatography ◽  
Low Density Lipoproteins ◽  
High Density ◽  
Plasma Lipoproteins ◽  
High Density Lipoproteins ◽  
Low Density ◽  
Very Low Density Lipoproteins ◽  
Simple Method ◽  
Lipoprotein Class

1. A simple method for isolation of individual human plasma lipoprotein classes is presented. In this technique, lipoproteins are removed from plasma at d1.225 by ultracentrifugation, after which they are separated and purified by agarose-column chromatography. 2. Three major classes are obtained after agarose-column chromatography. Separation between classes is excellent; more than 95% of the lipoproteins eluted from the column are recovered in the form of a purified lipoprotein class. 3. Each lipoprotein class was characterized immunologically, chemically, electrophoretically and by electron microscopy. A comparison of the properties of the column-isolated lipoproteins was made with very-low-density lipoproteins, low-density lipoproteins, and high-density lipoproteins separated by sequential ultracentrifugation at densities of 1.006, 1.063 and 1.21 respectively. 4. By each criterion, peak-I lipoproteins from the agarose column are the same as very-low-density lipoproteins, peak-II lipoproteins are the same as low-density lipoproteins, and peak-III lipoproteins are the same as high-density lipoproteins. Thus the lipoprotein classes isolated by both methods are similar if not identical. 5. The agarose-column separation technique offers the advantage of a two- to three-fold saving in time. In addition, the column-elution pattern serves as a recording of the size distribution of lipoproteins in plasma. 6. The most complete characterization is reported for human plasma lipoproteins. The results with rhesus-monkey and rabbit lipoproteins were identical.

scholarly journals Membrane receptors for very low density lipoprotein (VLDL) inhibitor of lymphocyte proliferation

Blood ◽  
1981 ◽  
Vol 57 (6) ◽  
pp. 1055-1064 ◽  
Author(s):  
PI Yi ◽  
G Beck ◽  
S Zucker
Keyword(s):  
Dna Synthesis ◽  
Lymphocyte Proliferation ◽  
Human Lymphocytes ◽  
Low Density Lipoproteins ◽  
Membrane Receptors ◽  
Plasma Lipoproteins ◽  
High Density Lipoproteins ◽  
Scatchard Analysis ◽  
Low Density ◽  
Very Low Density Lipoproteins

Abstract Physiologic concentrations of human plasma very low density lipoproteins inhibit the DNA synthesis of lymphocytes stimulated by allogeneic cells or lectins. In this report we have compared the effects of isolated lipoproteins [very low density lipoproteins (VLDL), low density lipoproteins (LDL), and high density lipoproteins (HDL)] and lipoprotein-depleted plasma (LDP) on DNA synthesis by phytohemagglutinin-stimulated human lymphocytes. The relative potency for the inhibition of lymphocyte proliferation was VLDL greater than LDL greater than HDL greater than LDP. Fifty percent inhibition of DNA synthesis was observed at a VLDL protein concentration of 1.5--2.0 microgram/ml. We have further demonstrated the presence of specific receptors for VLDL on human lymphocytes. Native VLDL was more effective than LDL in competing for 125I-VLDL binding sites. Subsequent to binding to lymphocytes, 125I-VLDL was internalized and degraded to acid- soluble products. Based on a Scatchard analysis of VLDL binding at 4 degrees C, the number of VLDL receptors per lymphocyte was estimated at 28,000 +/- 1300. Based on an estimated mean binding affinity for the VLDL receptor complex at half saturation of approximately 8.8 X 10(7) liter/mole, it is estimated that 91% of lymphocyte VLDL receptors are occupied at physiologic VLDL concentrations in blood. Although the immune regulatory role of plasma lipoproteins is uncertain, we suggest tha VLDL and LDL-In may maintain circulating blood lymphocytes in a nonproliferative state via their respective cell receptor mechanisms.

scholarly journals Membrane receptors for very low density lipoprotein (VLDL) inhibitor of lymphocyte proliferation

Blood ◽  
1981 ◽  
Vol 57 (6) ◽  
pp. 1055-1064
Author(s):  
PI Yi ◽  
G Beck ◽  
S Zucker
Keyword(s):  
Dna Synthesis ◽  
Lymphocyte Proliferation ◽  
Human Lymphocytes ◽  
Low Density Lipoproteins ◽  
Membrane Receptors ◽  
Plasma Lipoproteins ◽  
High Density Lipoproteins ◽  
Scatchard Analysis ◽  
Low Density ◽  
Very Low Density Lipoproteins

Physiologic concentrations of human plasma very low density lipoproteins inhibit the DNA synthesis of lymphocytes stimulated by allogeneic cells or lectins. In this report we have compared the effects of isolated lipoproteins [very low density lipoproteins (VLDL), low density lipoproteins (LDL), and high density lipoproteins (HDL)] and lipoprotein-depleted plasma (LDP) on DNA synthesis by phytohemagglutinin-stimulated human lymphocytes. The relative potency for the inhibition of lymphocyte proliferation was VLDL greater than LDL greater than HDL greater than LDP. Fifty percent inhibition of DNA synthesis was observed at a VLDL protein concentration of 1.5--2.0 microgram/ml. We have further demonstrated the presence of specific receptors for VLDL on human lymphocytes. Native VLDL was more effective than LDL in competing for 125I-VLDL binding sites. Subsequent to binding to lymphocytes, 125I-VLDL was internalized and degraded to acid- soluble products. Based on a Scatchard analysis of VLDL binding at 4 degrees C, the number of VLDL receptors per lymphocyte was estimated at 28,000 +/- 1300. Based on an estimated mean binding affinity for the VLDL receptor complex at half saturation of approximately 8.8 X 10(7) liter/mole, it is estimated that 91% of lymphocyte VLDL receptors are occupied at physiologic VLDL concentrations in blood. Although the immune regulatory role of plasma lipoproteins is uncertain, we suggest tha VLDL and LDL-In may maintain circulating blood lymphocytes in a nonproliferative state via their respective cell receptor mechanisms.

scholarly journals IMMUNOCHEMICAL STUDIES ON HUMAN PLASMA LIPOPROTEINS

1957 ◽  
Vol 105 (1) ◽  
pp. 49-67 ◽  
Author(s):  
Frederick Aladjem ◽  
Miriam Lieberman ◽  
John W. Gofman
Keyword(s):  
Human Plasma ◽  
Plasma Protein ◽  
Protein Fraction ◽  
Low Density Lipoproteins ◽  
High Density ◽  
Plasma Lipoproteins ◽  
High Density Lipoproteins ◽  
Low Density ◽  
Plasma Protein Fraction ◽  
Free Plasma

Low density human plasma lipoproteins Sf 17+, Sf 13, and Sf 6, high density lipoproteins 2 and 3, and a lipoprotein-free plasma protein fraction were isolated from human plasma by ultracentrifugal methods. It was found that human plasma lipoproteins are immunochemically distinct from the non-lipoprotein containing plasma protein fraction. Lipoprotein fractions of a given hydrated density, isolated from different individuals, were found to be immunochemically indistinguishable by qualitative absorption tests. Qualitative antigenic differences were shown to exist between low density lipoproteins and high density lipoproteins. Quantitative precipitin reactions showed that low density lipoproteins Sf 6 and Sf 13 were immunochemically very similar. However, they differed with respect to the amount of antigen nitrogen required for maximum precipitation. Agar diffusion analyses were performed; the results suggest heterogeneity of lipoproteins by this criterion.

A comparison of some immunological characteristics of very low density lipoproteins of normal and hypercholesterolemic rat sera

1978 ◽  
Vol 56 (6) ◽  
pp. 673-683 ◽  
Author(s):  
Peter J. Dolphin ◽  
Laurence Wong ◽  
David Rubinstein
Keyword(s):  
Polyacrylamide Gel Electrophoresis ◽  
Normal Serum ◽  
Low Density Lipoproteins ◽  
High Density Lipoproteins ◽  
Low Density ◽  
Very Low Density Lipoproteins ◽  
Rat Serum ◽  
Apo B ◽  
Apo E

The immunological characteristics of very low density lipoproteins (VLDL) from normal and hypercholesterolemic rat sera were compared using polyspecific antisera to VLDL and high density lipoproteins (HDL) and monospecific antisera to apo-B, apo-C, apo-A-I, and apo-E. Ultracentrifugally isolated VLDL from normal serum were studied by immunodiffusion and found to contain both discrete and associated (with apo-B) apo-C and apo-E, probably in the form of lipid-containing lipoproteins. However, immunoelectrophoresis of whole serum revealed only an associated form of the lipoprotein having pre-β mobility (i.e., VLDL), suggesting that the presence of discrete lipoproteins in isolated VLDL, each containing a single apoprotein family, may represent ultracentrifugal artifacts. Ultracentrifugally isolated VLDL from diet-induced hypercholesterolemic rat serum contained only trace amounts of apo-C and large quantities of apo-E, both of which were totally associated with apo-B. VLDL isolated by ultracentrifugation from perfusate of normal and hypercholesterolemic livers contained only associated lipoprotein complexes made up of apo-B, apo-C, and apo-E in the former but only apo-B and apo-E in the latter. These data suggest that normal VLDL are secreted as lipoprotein complexes containing apo-B, apo-C, and apo-E which may become destabilized in the circulation. However, VLDL from hypercholesterolemic serum show a marked diminution in the quantity of apo-C as indicated by the relative incorporation of [3H]leucine in vivo and by polyacrylamide gel electrophoresis of apo-VLDL.

Diagnosis of Type III Hyperlipoproteinemia by Chromatography of Plasma Lipoproteins on Columns Containing Agarose

1975 ◽  
Vol 21 (13) ◽  
pp. 1887-1891 ◽  
Author(s):  
James Shepherd ◽  
Christopher J Packard ◽  
Frances J Dryburgh ◽  
Jane L H C Third
Keyword(s):  
Low Density Lipoproteins ◽  
Plasma Lipoproteins ◽  
High Density Lipoproteins ◽  
Low Density ◽  
Very Low Density Lipoproteins ◽  
Type Iii ◽  
Elution Pattern ◽  
Type Iii Hyperlipoproteinemia ◽  
Primary Type ◽  
Relative Deficiency

Abstract Agarose column chromatography has been used to separate plasma lipoproteins into very-low-density lipoproteins (VLDL), low-density lipoproteins (LDL) and high-density lipoproteins (HDL). Applied to the diagnosis of primary type III hyperlipoproteinemia, the procedure is capable of demonstrating three characteristic and specific changes from normality in the elution pattern of lipoproteins from patients with this condition. In the type III profile there is (a) incomplete separation of VLDL from putative LDL material, (b) early elution of the type III LDL with respect to a normal LDL marker, and (c) relative deficiency of type III LDL with elution characteristics of normal LDL. We advocate the use of this method in the diagnosis of type III hyperlipoproteinemia.

Variability in Plasma Lipoprotein Profiles When Comparing Diltiazem and Propranolol

1993 ◽  
Vol 27 (9) ◽  
pp. 1048-1052
Author(s):  
Dustan G. Labreche ◽  
George T. Kondos ◽  
David W. Bartels ◽  
Jerry L. Bauman
Keyword(s):  
Drug Treatment ◽  
Comparative Trial ◽  
Low Density Lipoproteins ◽  
Plasma Lipoprotein ◽  
Plasma Lipoproteins ◽  
High Density Lipoproteins ◽  
Low Density ◽  
Very Low Density Lipoproteins ◽  
Double Blind ◽  
Propranolol Group

OBJECTIVE: To examine the effects of diltiazem and propranolol on plasma lipoproteins in a double-blind, comparative trial. PATIENTS: Twenty-one mild-to-moderate hypertensive patients. METHODS: Following discontinuation of previous antihypertensive treatments, and a 4-week, single-blind, placebo run-in, subjects were randomized to receive sustained-release diltiazem or propranolol. Total cholesterol, high-density lipoproteins (HDL), low-density lipoproteins (LDL), and very-low-density lipoproteins (VLDL) were measured during placebo administration and after 12–16 weeks of treatment. RESULTS: No significant changes in plasma lipoprotein concentrations were noted in either the diltiazem or propranolol group compared with baseline values or each other. Marked variation in HDL, LDL, and VLDL were noted following drug treatment and in eight subjects whose lipoprotein concentrations were remeasured prior to drug treatment during the placebo period. The alterations were bidirectional, and similar in magnitude to those found following drug treatment. CONCLUSIONS: In many cases, changes in plasma lipoproteins reported to be a consequence of antihypertensive treatment may merely reflect normal intrapatient variability.

scholarly journals Studies of the Proteins in Human Plasma Very Low Density Lipoproteins

1969 ◽  
Vol 244 (20) ◽  
pp. 5687-5694 ◽  
Author(s):  
W. Virgil Brown ◽  
Robert I. Levy ◽  
Donald S. Fredrickson
Keyword(s):  
Human Plasma ◽  
Low Density Lipoproteins ◽  
Low Density ◽  
Very Low Density Lipoproteins
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