Please use this identifier to cite or link to this item: https://scholarhub.balamand.edu.lb/handle/uob/7481
Title: The in vitro effect of myeloperoxidase oxidized LDL on THP-1 derived macrophages
Authors: Jeradeh, Elias
Frangie, Christian
Bazzi, Samer 
Daher, Jalil 
Affiliations: Faculty of Medicine 
Department of Biology 
Keywords: Atherosclerosis
Mox-LDL
Foam cells
THP-1
Macrophages
Issue Date: 2024-08-01
Publisher: Sage
Part of: Innate Immunity
Abstract: 
Cardiovascular diseases (CVDs) linked to atherosclerosis remains the leading cause of death worldwide. Atherosclerosis is primarily caused by the accumulation of oxidized forms of low density lipoprotein (LDL) in macrophages (MΦs) in the subendothelial layer of arteries leading to foam cell and fatty streak formation. Many studies suggest that LDL that is modified by myeloperoxidase (MPO) is a key player in the development of atherosclerosis. MΦs can adopt a variety of functional phenotypes that include mainly the proinflammatory M1 and the anti-inflammatory M2 MΦ phenotypes which are both implicated in the process of atherogenesis. In fact, MΦs that reside in atherosclerostic lesions were shown to express a variety of phenotypes ranging between the M1- and M2 MΦ types. Recently, we pointed out the involvement of MPO oxidized-LDL (Mox-LDL) in increasing inflammation in MΦs by reducing their secretion of IL-10. Since little is known about Mox-LDL-mediated pro-atherosclerostic responses in MΦs, our study aimed at analyzing the in vitro effects of Mox-LDL at this level through making use of the well-established model of human THP-1-derived Mφs. Our results demonstrate that Mox-LDL has no effect on apoptosis, reactive oxygen species (ROS) generation and cell death in our cell model; yet, interestingly, our results show that Mox-LDL is significantly engulfed at a higher rate in the different MΦ subtypes supporting its key role in foam cell formation during the progression of the disease as well as previous data that were generated using another primary MΦ cell model of atherosclerosis.
URI: https://scholarhub.balamand.edu.lb/handle/uob/7481
ISSN: 17534259
DOI: 10.1177/17534259241269687
Ezproxy URL: Link to full text
Type: Journal Article
Appears in Collections:Department of Biology
Faculty of Medicine

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