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Novel Insights into the Link Between Myeloperoxidase Modified LDL, LOX-1, and Neuroserpin in Stroke

Layal El-Hajjar1, Elena Miranda2, Marwan El-Sabban1

  • 1Department of Anatomy, Cell Biology and Physiological Sciences, Faculty of Medicine, American University of Beirut, 1107 Beirut, Lebanon.

Reviews in Cardiovascular Medicine
|July 30, 2024
PubMed

Insights

Myeloperoxidase oxidized LDL (Mox-LDL) impairs endothelial cell fibrinolysis by increasing neuroserpin, but the lectin-like oxidized LDL receptor-1 (lox-1) mitigates this effect. Lox-1 protects against Mox-LDL-induced decreases in fibrinolytic capacity, impacting stroke risk.

Area of Science:

  • Cardiovascular Research
  • Endothelial Cell Biology
  • Atherosclerosis Pathophysiology

Background:

  • Atherosclerosis, a major cause of global mortality, stems from endothelial dysfunction and modified LDL accumulation.
  • Myeloperoxidase oxidized LDL (Mox-LDL) is implicated in atherosclerosis, potentially through binding to the lectin-like oxidized LDL receptor-1 (lox-1) and promoting inflammation.
  • Neuroserpin, a serine proteinase inhibitor, plays a role in fibrinolysis within nervous tissue.

Purpose of the Study:

  • To investigate the in vitro effects of Mox-LDL on the fibrinolytic activity of human aortic endothelial cells (HAECs).
  • To determine the role of the lox-1 scavenger receptor in mediating Mox-LDL's impact on endothelial fibrinolysis.
  • To assess neuroserpin expression and release in response to Mox-LDL and lox-1 activity.

Main Methods:

  • Utilized lox-1 gene silencing in HAECs to evaluate the receptor's role.
  • Cultured cells with Mox-LDL and measured neuroserpin expression via qPCR and ELISA.
  • Assessed endothelial cell fibrinolytic activity using the Euglobulin Clot Lysis Time (ECLT) method.

Main Results:

  • Mox-LDL was found to decrease endothelial cell fibrinolytic capacity.
  • This decrease in fibrinolytic capacity was associated with increased neuroserpin levels in lox-1 knockdown cells.
  • Upregulation of neuroserpin correlated with reduced fibrinolytic activity.

Conclusions:

  • The lectin-like oxidized LDL receptor-1 (lox-1) plays a protective role for endothelial cells against Mox-LDL.
  • Lox-1 mitigates Mox-LDL-induced reductions in pro-fibrinolytic capacity.
  • These findings have significant implications for understanding stroke pathogenesis and potential therapeutic targets.
Abstract

Keywords:
Mox-LDLatherosclerosisendothelial dysfunctionlox-1neuroserpinstroke

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