Model class A and class L peptides increase the production of apoA-I-containing lipoproteins in HepG2 cells

Class A peptides inhibit atherosclerosis and protect cells from class L peptide-mediated lysis. Because the cytolytic process is concentration dependent, we hypothesized that at certain concentrations both classes of peptides exert similar effect(s) on cells. To test this hypothesis, we studied the...

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Main Authors: Nassrin Dashti, Geeta Datta, Medha Manchekar, Manjula Chaddha, G.M. Anantharamaiah
Format: Article
Language:English
Published: Elsevier 2004-10-01
Series:Journal of Lipid Research
Subjects:
Online Access:http://www.sciencedirect.com/science/article/pii/S0022227520312669
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author Nassrin Dashti
Geeta Datta
Medha Manchekar
Manjula Chaddha
G.M. Anantharamaiah
author_facet Nassrin Dashti
Geeta Datta
Medha Manchekar
Manjula Chaddha
G.M. Anantharamaiah
author_sort Nassrin Dashti
collection DOAJ
description Class A peptides inhibit atherosclerosis and protect cells from class L peptide-mediated lysis. Because the cytolytic process is concentration dependent, we hypothesized that at certain concentrations both classes of peptides exert similar effect(s) on cells. To test this hypothesis, we studied the effects of a class L peptide (18L = GIKKFLGSIWKFIKAFVG) and a class A peptide, 18A-Pro-18A (18A = DWLKAFYDKVAEKLKEAF) (37pA), on apolipoprotein and lipoprotein production in HepG2 cells. Secretion of 35S-labeled apolipoprotein A-I (apoA-I) was stimulated by both 18L (110%) and 37pA (135%) at 10 and 20 nM of peptides, respectively. Both peptides enhanced the secretion of 3H-labeled phospholipids by 140% and 14C-labeled HDL-cholesterol (HDL-C) by 35% but had no significant effect on the total cholesterol mass or secretion.These results indicate that class L and class A peptides cause redistribution of cholesterol among lipoproteins in favor of HDL-C. Both peptides remodeled apoA-I-containing particles forming preβ- as well as α-HDL. This study suggests that increased secretion of phospholipids and apoA-I and the formation of preβ-HDL particles might contribute to the antiatherogenic properties of these peptides.
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spelling doaj.art-ef6502b3689f43c98f95731f477333612022-12-21T18:55:45ZengElsevierJournal of Lipid Research0022-22752004-10-01451019191928Model class A and class L peptides increase the production of apoA-I-containing lipoproteins in HepG2 cellsNassrin Dashti0Geeta Datta1Medha Manchekar2Manjula Chaddha3G.M. Anantharamaiah4Department of Medicine, Biochemistry, and Molecular Genetics, and Atherosclerosis Research Unit, University of Alabama at Birmingham, Birmingham, AL 35294Department of Medicine, Biochemistry, and Molecular Genetics, and Atherosclerosis Research Unit, University of Alabama at Birmingham, Birmingham, AL 35294Department of Medicine, Biochemistry, and Molecular Genetics, and Atherosclerosis Research Unit, University of Alabama at Birmingham, Birmingham, AL 35294Department of Medicine, Biochemistry, and Molecular Genetics, and Atherosclerosis Research Unit, University of Alabama at Birmingham, Birmingham, AL 35294Department of Medicine, Biochemistry, and Molecular Genetics, and Atherosclerosis Research Unit, University of Alabama at Birmingham, Birmingham, AL 35294Class A peptides inhibit atherosclerosis and protect cells from class L peptide-mediated lysis. Because the cytolytic process is concentration dependent, we hypothesized that at certain concentrations both classes of peptides exert similar effect(s) on cells. To test this hypothesis, we studied the effects of a class L peptide (18L = GIKKFLGSIWKFIKAFVG) and a class A peptide, 18A-Pro-18A (18A = DWLKAFYDKVAEKLKEAF) (37pA), on apolipoprotein and lipoprotein production in HepG2 cells. Secretion of 35S-labeled apolipoprotein A-I (apoA-I) was stimulated by both 18L (110%) and 37pA (135%) at 10 and 20 nM of peptides, respectively. Both peptides enhanced the secretion of 3H-labeled phospholipids by 140% and 14C-labeled HDL-cholesterol (HDL-C) by 35% but had no significant effect on the total cholesterol mass or secretion.These results indicate that class L and class A peptides cause redistribution of cholesterol among lipoproteins in favor of HDL-C. Both peptides remodeled apoA-I-containing particles forming preβ- as well as α-HDL. This study suggests that increased secretion of phospholipids and apoA-I and the formation of preβ-HDL particles might contribute to the antiatherogenic properties of these peptides.http://www.sciencedirect.com/science/article/pii/S0022227520312669apolipoprotein A-Iapolipoprotein Bhigh density lipoprotein metabolismlow density lipoprotein metabolismtriglyceride secretioncholesterol secretion
spellingShingle Nassrin Dashti
Geeta Datta
Medha Manchekar
Manjula Chaddha
G.M. Anantharamaiah
Model class A and class L peptides increase the production of apoA-I-containing lipoproteins in HepG2 cells
Journal of Lipid Research
apolipoprotein A-I
apolipoprotein B
high density lipoprotein metabolism
low density lipoprotein metabolism
triglyceride secretion
cholesterol secretion
title Model class A and class L peptides increase the production of apoA-I-containing lipoproteins in HepG2 cells
title_full Model class A and class L peptides increase the production of apoA-I-containing lipoproteins in HepG2 cells
title_fullStr Model class A and class L peptides increase the production of apoA-I-containing lipoproteins in HepG2 cells
title_full_unstemmed Model class A and class L peptides increase the production of apoA-I-containing lipoproteins in HepG2 cells
title_short Model class A and class L peptides increase the production of apoA-I-containing lipoproteins in HepG2 cells
title_sort model class a and class l peptides increase the production of apoa i containing lipoproteins in hepg2 cells
topic apolipoprotein A-I
apolipoprotein B
high density lipoprotein metabolism
low density lipoprotein metabolism
triglyceride secretion
cholesterol secretion
url http://www.sciencedirect.com/science/article/pii/S0022227520312669
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