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Effect of myeloperoxidase modified LDL on bovine and human aortic endothelial cells
Ghadir El Samad1, Samer Bazzi1, Marc Karam1
1Department of Biology, Faculty of Sciences, University of Balamand, Tripoli 100, Lebanon.
Insights
Myeloperoxidase-modified LDL (MoxLDL) does not alter fibrinolysis in human aortic endothelial cells. However, MoxLDL and copper-oxidized LDL (CuoxLDL) show different effects on endothelial cells, offering potential drug targets for atherosclerosis.
Area of Science:
- Cardiovascular Biology
- Endothelial Cell Function
- Atherosclerosis Pathogenesis
Background:
- Atherosclerosis, a major cause of death, involves endothelial cell dysfunction and oxidized LDL accumulation.
- Decreased endothelial cell fibrinolysis is linked to atheroma plaque formation.
- Myeloperoxidase-modified LDL (MoxLDL) has been shown to reduce endothelial cell profibrinolytic capacity.
Purpose of the Study:
- To investigate MoxLDL's role in endothelial cell dysfunction.
- To identify molecules involved in MoxLDL-induced decrease in human aortic endothelial cell (HAEC) fibrinolysis.
- To compare HAEC and bovine aortic endothelial (BAE) cell responses to MoxLDL and assess reactive oxygen species (ROS) generation.
Main Methods:
- Reverse transcription-quantitative PCR to screen for differential gene expression in the fibrinolytic process.
- Treatment of HAEC and BAE cells with MoxLDL.
- Measurement of reactive oxygen species (ROS) generation.
Main Results:
- MoxLDL treatment did not alter the expression of major fibrinolytic factors in HAEC.
- A notable discrepancy was observed in the response of HAEC and BAE cells to modified LDL.
- MoxLDL did not increase ROS generation in HAEC, unlike copper-oxidized LDL (CuoxLDL).
Conclusions:
- MoxLDL does not directly impact major fibrinolytic factors in HAEC.
- Differential responses of HAEC and BAE cells to modified LDL warrant further investigation.
- Understanding MoxLDL and CuoxLDL effects on endothelial cells may reveal novel therapeutic targets for atherosclerosis.
Abstract:
Cardiovascular disease associated with atherosclerosis is a leading cause of death worldwide. Atherosclerosis is primarily caused by the dysfunction of vascular endothelial cells and the subendothelial accumulation of oxidized forms of low-density lipoproteins (LDL). Early observations have associated fibrin deposition with atheroma plaque formation, which has led to the proposition that a decrease in endothelial cell fibrinolysis may negatively influence atherogenesis. It has been recently demonstrated that myeloperoxidase modified LDL (MoxLDL) decreases endothelial cell profibrinolytic capacity in real-time. The present study investigated the role of MoxLDL in endothelial cell dysfunction by determining the molecules that may be involved in decreasing the fibrinolysis of human aortic endothelial cells (HAEC). Accordingly, reverse transcription-quantitative PCR was performed to screen for the differential expression of major genes that are implicated in the fibrinolytic process. In addition, the response of the latter cell type to MoxLDL was compared with bovine aortic endothelial (BAE) cells. Furthermore, the effect of the treatment on the generation of reactive oxygen species (ROS) was also determined. Although the current study did not demonstrate an association between MoxLDL treatment and a change in the expression of any major fibrinolytic factor in HAEC, a discrepancy between HAEC and BAE cells with respect to their response to modified LDL treatment was observed. The result have also demonstrated that MoxLDL does not increase ROS generation in HAEC as opposed to the other major type of modified LDL, cupper oxidized LDL (CuoxLDL) that was reported to exhibit a positive effect at this level. The present study provided important insight into the different effects of MoxLDL and CuoxLDL in endothelial cells, which may aid future studies to determine the various signaling pathways that are promoted by these molecules. The results of the present study may be utilized to identify potential molecular drug targets for the treatment of atherosclerosis.
