Open AccessLow Doses of Innate Defence Regulator Peptide, IDR-1018, Enhances HDL-Mediated Cholesterol Efflux from Smooth Muscle Cells and Macrophages
Author(s) -
Afacan Nj,
Teddy Chan,
Jelena Pistolic,
Jennifer Y. Kong,
Francis Ga,
R.L. Hancock
Publication year - 2016
Publication title -
journal of nutritional biology
Language(s) - English
Resource type - Journals
ISSN - 2469-4142
DOI - 10.18314/jnb.v2i1.110
Subject(s) - abca1 , efflux , cholesterol , apolipoprotein b , regulator , reverse cholesterol transport , intracellular , lipoprotein , chemistry , peptide , microbiology and biotechnology , high density lipoprotein , pharmacology , transporter , biochemistry , biology , gene
Cardiovascular diseases due to atherosclerosis are the leading cause of death worldwide. In recent years, novel therapeutics designed to enhance high-density lipoprotein (HDL) activity as a treatment for atherosclerosis have been explored. Of particular interest is the use of amphipathic α-helical peptides to mimic the action of the main HDL protein, apolipoprotein (Apo)AI. Immunomodulatory peptides share many physical and functional
properties with ApoAI and its mimetics; we therefore hypothesized that they too might be capable of enhancing cholesterol efflux. The aim of this study was to determine whether a potent immunomodulatory peptide, innate defence regulator (IDR)-1018, could promote cholesterol efflux from cells. Here, we report that IDR-1018 induced a dose-dependent increase in ApoAI on the cell surface and ATP-binding cassette transporter A1 (ABCA1)
protein levels. Functional assays revealed that low doses of IDR-1018 improved HDL-mediated suppression of intracellular cholesteryl ester accumulation in macrophages and enhanced HDL-mediated cellular cholesterol efflux from smooth muscle cells and macrophages. Based on these results we propose that natural and synthetic immunomodulatory peptides like IDR-1018 represent a large new group of peptides that could be developed for
the treatment of atherosclerosis.