Please use this identifier to cite or link to this item: https://scholarhub.balamand.edu.lb/handle/uob/7201
Title: Novel Insights into the Link Between Myeloperoxidase Modified LDL, LOX-1, and Neuroserpin in Stroke
Authors: El-Hajjar, Layal
Miranda, Elena
El-Sabban, Marwan
Daher, Jalil 
Affiliations: Department of Biology 
Keywords: Atherosclerosis
Stroke
Mox-LDL
Neuroserpin
Endothelial dysfunction
lox-1
Issue Date: 2023-12-15
Publisher: IMR Press
Part of: Reviews in Cardiovascular Medicine
Volume: 24
Issue: 12
Abstract: 
Background: Cardiovascular disease that is caused by atherosclerosis is the leading cause of death worldwide. Atherosclerosis is primarily triggered by endothelial dysfunction and the accumulation of modified low-density lipoprotein (LDL) particles in the subendothelial space of blood vessels. Early reports have associated oxidized LDL with altered fibrinolysis and atherogenesis. It has been suggested that myeloperoxidase oxidized LDL (Mox-LDL) is involved in atherosclerosis because of its significant pathophysiological role in the modification of LDL in vivo. It has been equally demonstrated that Mox-LDL binds to the lectin-like oxidized low-density lipoprotein receptor-1 (lox-1) scavenger receptor which leads to the upregulation of inflammatory mediators in endothelial cells and the progression of cardiovascular disease. It has been also shown that neuroserpin, a member of the serine proteinase inhibitor (serpin) superfamily, has an important role at the level of fibrinolysis in the nervous tissue. Methods: Since little is known about the effects of Mox-LDL on endothelial cell fibrinolytic activity and the involvement of lox-1 in this process, our study aimed at evaluating the in vitro effects of Mox-LDL on neuroserpin release from human aortic endothelial cells (HAECs) and the role of lox-1 scavenger receptor in this context by relying on lox-1 gene silencing in HAECs, culturing the cells in the presence of Mox-LDL, measuring their neuroserpin expression and release by quantitative polymerase chain reaction (qPCR) and enzyme-linked immunosorbent assay (ELISA), respectively, and assessing their fibrinolytic activity using the Euglobulin Clot Lysis Time (ECLT) method. Results: Our data show that Mox-LDL decreases endothelial cell fibrinolytic capacity by upregulating neuroserpin in lox-1 knockdown cells. Conclusions: Lox-1 protects the endothelial cells from a Mox-LDL-induced decrease in pro-fibrinolytic capacity, which has important consequences in the context of stroke.
URI: https://scholarhub.balamand.edu.lb/handle/uob/7201
DOI: 10.31083/j.rcm2412354
Open URL: Link to full text
Type: Journal Article
Appears in Collections:Department of Biology

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