Increased expression of endothelial lipase in symptomatic and unstable carotid plaques

Matias Trbušić1, Monika Riederer, Majda Vučić

  • 1University of Zagreb School of Medicine, Zagreb, Croatia.

Journal of Neurology
|August 16, 2011
PubMed

Insights

Endothelial lipase (EL) protein expression is higher in unstable human carotid artery plaques (HCAP) and associated with symptoms. This suggests EL may indicate or drive plaque instability and related symptoms.

Area of Science:

  • Cardiovascular Research
  • Atherosclerosis Research
  • Biomarker Discovery

Background:

  • Advanced human carotid artery plaques (HCAP) are a significant cause of stroke.
  • Plaque instability is a key factor in cerebrovascular events.
  • Endothelial lipase (EL) is implicated in lipid metabolism and inflammation.

Purpose of the Study:

  • To investigate the relationship between endothelial lipase (EL) protein expression and the instability of advanced human carotid artery plaques (HCAP).
  • To determine if EL expression correlates with symptoms in patients with HCAP.
  • To explore the localization of EL within HCAP.

Main Methods:

  • HCAP samples were obtained from 66 patients undergoing carotid endarterectomy (CEA).
  • Plaque instability was assessed using ultrasound and histological analysis.
  • EL protein expression was quantified via immunostaining and scored semi-quantitatively.
  • Monocyte and macrophage markers (CD163) were used to identify inflammatory cells.

Main Results:

  • High EL staining was significantly more common in histologically unstable plaques (p=0.004).
  • Elevated EL expression was observed in symptomatic patients compared to asymptomatic individuals (p=0.028).
  • EL immunostaining predominantly co-localized with CD163-positive macrophages.

Conclusions:

  • Endothelial lipase (EL) expression is associated with increased instability in human carotid artery plaques (HCAP).
  • EL may serve as a potential biomarker for HCAP instability and symptomatology.
  • EL's presence in macrophages suggests a role in the inflammatory processes driving plaque vulnerability.

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