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The in vitro effect of myeloperoxidase oxidized LDL on THP-1 derived macrophages
Elias Jeradeh1, Christian Frangie2, Samer Bazzi3
1Department of Biology, Faculty of Arts and Sciences, University of Balamand, El-Koura, Lebanon.
Insights
Myeloperoxidase oxidized-LDL (Mox-LDL) is readily engulfed by macrophages, promoting foam cell formation. This study found Mox-LDL does not increase cell death or reactive oxygen species in macrophages, but enhances its uptake, a key step in atherosclerosis development.
Area of Science:
- Cardiovascular Biology
- Immunology
- Atherosclerosis Research
Background:
- Cardiovascular diseases (CVDs) are the leading global cause of death, primarily driven by atherosclerosis.
- Atherosclerosis involves oxidized low-density lipoprotein (LDL) accumulation in macrophages, leading to foam cell formation.
- Myeloperoxidase (MPO)-modified LDL (Mox-LDL) is implicated in promoting pro-atherosclerotic inflammatory responses in macrophages.
Purpose of the Study:
- To investigate the in vitro effects of Mox-LDL on human THP-1-derived macrophages.
- To analyze Mox-LDL's role in macrophage apoptosis, reactive oxygen species (ROS) generation, and cell death.
- To determine Mox-LDL uptake rates across different macrophage subtypes.
Main Methods:
- Utilized a well-established in vitro model of human THP-1-derived macrophages.
- Assessed the impact of Mox-LDL on macrophage apoptosis, ROS generation, and cell death.
- Quantified Mox-LDL engulfment by various macrophage phenotypes.
Main Results:
- Mox-LDL did not significantly affect apoptosis, ROS generation, or cell death in the studied macrophage model.
- Macrophages demonstrated a significantly higher rate of Mox-LDL engulfment across different subtypes.
- These findings support Mox-LDL's crucial role in foam cell formation during atherosclerosis progression.
Conclusions:
- Mox-LDL is readily taken up by macrophages, contributing to foam cell formation, a critical step in atherosclerosis.
- Mox-LDL does not induce cell death or oxidative stress in this macrophage model.
- Further research into Mox-LDL's specific pro-atherosclerotic mechanisms in macrophages is warranted.
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.
