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Regulation of oxidized platelet lipidome: implications for coronary artery disease

Madhumita Chatterjee1, Dominik Rath1, Jörg Schlotterbeck2

  • 1Department of Cardiology and Cardiovascular Medicine, Universität Tübingen, Otfried-Müller-Strasse 10, 72076 Tübingen, Germany.

European Heart Journal
|April 22, 2017
PubMed

Insights

Altered platelet lipidome in coronary artery disease (CAD) patients contributes to thrombosis. The CXCL12-CXCR4-CXCR7 axis may regulate this process, impacting platelet function and thrombotic risk.

Area of Science:

  • Cardiovascular Biology
  • Platelet Physiology
  • Lipid Metabolism

Background:

  • Hyperlipidaemia increases thrombosis risk, and oxidized LDL (oxLDL) binding to platelets in acute coronary syndrome (ACS) correlates with activation.
  • Platelet lipid profiles in symptomatic coronary artery disease (CAD) patients are not well understood.

Purpose of the Study:

  • To investigate the platelet lipidome in symptomatic CAD patients.
  • To explore the functional consequences of the chemokine CXCL12 and its receptors CXCR-4/-7 on platelet lipid uptake.

Main Methods:

  • Flow cytometry to detect platelet-oxLDL and CXCR4/7 expression.
  • Liquid chromatography-high-resolution mass spectrometry for lipidomic analysis.
  • Calibrated automated thrombinoscopy and live imaging microscopy to assess platelet function.
  • In vivo mouse models of thrombosis.

Main Results:

  • Platelet-oxLDL was elevated in CAD patients and correlated with CXCR7 and inversely with CXCR4 expression.
  • Intracoronary thrombi in ACS patients showed oxLDL deposition in platelet-rich areas.
  • LDL-oxLDL uptake increased oxidative stress, lipid peroxidation, and platelet activation (degranulation, integrin activation, apoptosis, thrombin generation).
  • LDL-oxLDL enhanced thrombus formation in vitro and in vivo.
  • CXCL12 modulated LDL-oxLDL uptake and augmented its pro-thrombotic effects.

Conclusions:

  • An altered platelet lipidome is associated with thrombotic risk in CAD.
  • The CXCL12-CXCR4-CXCR7 axis may be a key regulator of this mechanism in platelets.
Abstract

Keywords:
ChemokinesCoronary artery diseaseLipidomicsPlateletThrombus

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