Increase in circulating ACE-positive endothelial microparticles during acute lung injury

Eur Respir J. 2019 Oct 17;54(4):1801188. doi: 10.1183/13993003.01188-2018. Print 2019 Oct.

Abstract

Circulating endothelial microparticles (EMPs) are considered to be markers of endothelial injury, and lung microvascular endothelial cells express higher levels of angiotensin-converting enzyme (ACE). The aim of this study is to examine whether the number of ACE+ microvascular EMPs could be a prognostic marker for the development of acute respiratory distress syndrome (ARDS) in septic patients.The numbers of EMPs and ACE+ EMPs in the culture supernatant from human microvascular endothelial cells, as well as in the blood of mouse lung injury models and septic patients (n=82), were examined using flow cytometry.ACE+ EMPs in the culture supernatant from pulmonary microvascular endothelial cells increased after exposure to an inflammatory stimulus. In the mouse lung injury models, the circulating ACE+ EMPs and ACE+ EMP/EMP ratio were higher than in the controls (p<0.001). The ACE+ EMP/EMP ratio was correlated with the wet/dry lung ratio (rs=0.775, p<0.001). The circulating ACE+ EMPs and ACE+ EMP/EMP ratio on admission were significantly increased in septic patients who developed ARDS compared with septic patients who did not (p<0.001).Therefore, circulating ACE+ EMPs may be a prognostic marker for the development of ARDS in the septic patients.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acute Lung Injury / metabolism*
  • Aged
  • Animals
  • Cell-Derived Microparticles / metabolism*
  • Disease Models, Animal
  • Endothelial Cells / metabolism*
  • Female
  • Humans
  • Male
  • Mice
  • Middle Aged
  • Peptidyl-Dipeptidase A / metabolism*
  • Prognosis
  • Prospective Studies
  • Respiratory Distress Syndrome / etiology
  • Respiratory Distress Syndrome / metabolism*
  • Sepsis / complications
  • Sepsis / metabolism
  • Shock, Septic / complications
  • Shock, Septic / metabolism*

Substances

  • Peptidyl-Dipeptidase A