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Matrix metalloproteinase-9 might affect adaptive immunity in non-ST segment elevation acute coronary syndromes by

Giulia Angelini1, Davide Flego1, Ramona Vinci1

  • 1Department of Cardiovascular and Thoracic Sciences, Catholic University of the Sacred Heart, Fondazione Policlinico Universitario A. Gemelli, Largo A. Gemelli, 8-00168 Rome, Italy.

European Heart Journal
|December 7, 2017
PubMed

Insights

Matrix metalloproteinase-9 (MMP-9) enhances CD31 cleavage in CD4+ T-cells of acute coronary syndrome (ACS) patients. Inhibiting MMP-9 may offer a therapeutic target for T-cell dysregulation in ACS.

Area of Science:

  • Immunology
  • Cardiovascular Medicine
  • Molecular Biology

Background:

  • Adaptive immunity dysregulation, indicated by effector T-cell activity, may contribute to coronary instability in acute coronary syndrome (ACS).
  • Cleavage and shedding of the functional CD31 domain 1-5 are linked to uncontrolled lymphocyte activation.
  • Matrix metalloproteinase-9 (MMP-9) is implicated in CD31 cleavage and elevated in ACS patients.

Purpose of the Study:

  • To investigate the mechanisms of CD31 dysregulation in ACS.
  • To determine the role of MMP-9 in CD31 cleavage on T-cells in ACS patients.

Main Methods:

  • Flow cytometry was used to analyze CD31 cleavage on CD4+ T-cells from ACS patients, stable angina (SA) patients, and controls (CTRL).
  • Two CD31 antibodies were employed to differentiate between functional (domain 1-5) and non-functional (domain 6) epitopes.
  • ELISA was used to measure MMP-9 production in T-cell supernatants.

Main Results:

  • The ratio of CD31 functional domain 1-5 to domain 6 was significantly lower in ACS patients compared to SA and CTRL groups.
  • This ratio remained lower in ACS patients even after T-cell stimulation.
  • Elevated MMP-9 production was observed in stimulated CD4+ T-cells from ACS patients, and MMP-9 inhibition reduced CD31 domain 1-5 expression.

Conclusions:

  • Enhanced MMP-9 release is a key factor in the cleavage and shedding of the functional CD31 domain 1-5 on CD4+ T-cells in ACS patients.
  • This MMP-9-mediated CD31 cleavage represents a potential therapeutic target for modulating T-cell dysregulation in ACS.
Abstract

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