Endothelial damage effects of circulating microparticles from patients with stable angina are reduced by aspirin

Gong Cheng1, Xue-Feng Shan2, Xu-Lang Wang3

  • 1Department of Cardiology, Shaanxi Provincial People's Hospital, Xi'an, Shaanxi, China.

Abstract

Insights

Aspirin reduces pro-inflammatory circulating microparticles (MPs) in stable angina patients, impacting pathways involved in cardiovascular disease. This clarifies aspirin's effects beyond its anti-clotting role.

Area of Science:

  • Cardiovascular Medicine
  • Biochemistry
  • Pharmacology

Background:

  • Platelet activation is key in coronary artery disease (CAD) and circulating microparticles (MPs) formation.
  • The effect of aspirin, a common CAD treatment, on MP function is not well understood.

Purpose of the Study:

  • To investigate how aspirin affects MPs from healthy subjects and stable angina (SA) patients.
  • To determine the impact of MPs, with and without aspirin, on specific signaling pathways in rat thoracic aortas.

Main Methods:

  • Collected MPs from healthy individuals and SA patients before and after aspirin treatment.
  • Utilized flow cytometry to identify MP origins.
  • Incubated rat thoracic aortas with MPs (± aspirin) and measured expression of ERK1/2, JNKs, p38 MAPK, NF-κB, VCAM-1, NO, and O2-.

Main Results:

  • SA patients had higher MP levels, which decreased after aspirin; aspirin primarily reduced platelet-derived MPs.
  • MPs from SA patients altered signaling pathways, increasing p38 MAPKs, JNKs, NF-κB, VCAM-1, and O2-, while decreasing ERK1/2 and NO.
  • Aspirin treatment inhibited these pro-inflammatory MP functions, similar to pathway-specific inhibitors.

Conclusions:

  • Aspirin partially blocks the pro-inflammatory, oxidative stress, procoagulant, and adhesion properties of MPs.
  • This occurs via the ERK-NO/O2- and p38 -NF-κB-VCAM-1 signaling pathways.
  • These findings reveal functions of aspirin beyond its anti-atherothrombotic effects.

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