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Journal of Lipids
Volume 2017, Article ID 8479482, 9 pages
https://doi.org/10.1155/2017/8479482
Research Article

Elucidation of the Role of Lectin-Like oxLDL Receptor-1 in the Metabolic Responses of Macrophages to Human oxLDL

1Department of Chemistry, Vanderbilt University, VU Station B, Nashville, TN 37235-1822, USA
2Vanderbilt Institute for Integrative Biosystems Research and Education, Vanderbilt University, Nashville, TN 37235-1809, USA
3Novartis Institutes for Biomedical Research, 220 Massachusetts Ave. 360C, Cambridge, MA 02139, USA

Correspondence should be addressed to David E. Cliffel; ude.tlibrednav@leffilc.d

Received 13 February 2017; Accepted 4 May 2017; Published 31 May 2017

Academic Editor: Zufeng Ding

Copyright © 2017 Danielle W. Kimmel et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Atherogenesis is the narrowing of arteries due to plaque build-up that results in cardiovascular disease that can lead to death. The macrophage lectin-like oxidized LDL receptor-1 (LOX-1), also called the oxidized low-density lipoprotein receptor 1 (OLR1), is currently thought to aid in atherosclerotic disease progression; therefore metabolic studies have potential to both provide mechanistic validation for the role of LOX-1 in disease progression and provide valuable information regarding biomarker strategies and clinical imaging. One such mechanistic study is the upregulation of LOX-1 by methylated bacterial DNA and deoxy-cytidylate-phosphate-deoxy-guanylate-DNA (CpG)-DNA exposure. CpG-DNA is known to promote oxidative burst responses in macrophages, due to its direct binding to toll-like receptor 9 (TLR9) leading to the initiation of an NF-κB mediated immune response. In addition to the upregulation of macrophage LOX-1 expression, these studies have also examined the macrophage metabolic response to murine LOX-1/OLR1 antibody exposure. Our data suggests the antibody exposure effectively blocks LOX-1 dependent oxLDL metabolic activation of the macrophage, which was quantified using the multianalyte microphysiometer (MAMP). Using the MAMP to examine metabolic fluctuations during various types of oxLDL exposure, LOX-1 upregulation and inhibition provide valuable information regarding the role of LOX-1 in macrophage activation of oxidative burst.