J. Lipid Res. Neurobiology of Lipids (ISSN1683-5506)
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A more recent version of this article appeared on October 1, 2004

Papers In Press, published online ahead of print August 1, 2004
J. Lipid Res., doi:10.1194/jlr.M400251-JLR200
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Submitted on July 2, 2004
Revised on August 1, 2004
Accepted on July 16, 2004

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

Nassrin Dashti, Geeta Datta, Medha Manchekar, Manjula Chaddha, and G.M. Anantharamaiah

Medicine, University of Alabama at Birmingham, Birmingham, AL 35297-0012

Corresponding Author: ndashti{at}uab.edu

Class A peptides inhibit atherosclerosis and protect cells from class L peptide-mediated lysis. Since the cytolytic process is concentration dependent, we hypothesized that under 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 = DWLKAFYDKVAEK-LKEAF) (37pA) on apolipoprotein (apo) and lipoprotein production in HepG2 cells. Secretion of [35S]-labeled apoA-I was stimulated by both 18L (110%) and 37pA (135%) at 10 nM and 20 nM of peptides, respectively. Both peptides enhanced the secretion of [3H]-labeled phospholipids (PL) by 140% and [14C]-labeled high density lipoprotein (HDL) cholesterol (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 preß- as well as a-HDL. This study suggests that increased secretion of PL and apoA-I and the formation of preß particles might contribute to the antitherogenic properties of these peptides.


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