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The pericardium promotes cardiac repair and remodelling post-myocardial infarction

Research output: Contribution to journalJournal article

Unpublished
  • Katie Mylonas
  • Lucy Jackson-Jones
  • Jack Andrews
  • Marlene Magalhaes
  • Marco Meloni
  • Nikhil Joshi
  • Judith Allen
  • David Newby
  • Marc Dweck
  • Gillian Gray
  • Cecile Benezech
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<mark>Journal publication date</mark>18/09/2019
<mark>Journal</mark>Biorxiv
Publication StatusUnpublished
<mark>Original language</mark>English

Abstract

The pericardium is widely recognised for its lubricating and bio-mechanical properties. It also contains fat-associated lymphoid clusters (FALCs) and its immune functions have been widely overlooked. Here we aimed to assess the inflammatory activity of the pericardium in patients who suffered a recent myocardial infarction (MI) and to determine its importance for repair and remodelling in a murine MI model induced by coronary artery ligation (CAL). By comparing 18F-fluorodeoxyglucose (FDG) activity in the pericardium of patients with stable coronary artery disease and patients who had a recent MI, we demonstrate that MI is associated with increased pericardial inflammation. We confirm in mice, that pericardial FALCs undergo a major expansion following CAL. We show that despite similar initial injury, removal of the pericardium prior to MI disrupted subsequent repair, resulting in 50% mortality due to cardiac rupture, while all mice with intact pericardia survived. Removal of the pericardium also led to decreased staining for Ym1, a marker of reparative macrophages and adverse cardiac fibrosis within the infarct area. Together, this work indicates a crucial role for the pericardium in regulating inflammation, macrophage polarisation and tissue remodelling in the heart following MI.