Elevated Circulatory Levels of UL16 Binding Protein 1 Positive Microparticles Are Associated With Acute Myocardial

Songpol Haohan1,2,3, Burabha Pussadhamma1,4, Amonrat Jumnainsong2,3

  • 1Cardiovascular Research Group, Khon Kaen University, Khon Kaen, Thailand.

In Vivo (Athens, Greece)
|October 30, 2024
PubMed

Insights

Elevated ULBP1+ microparticles (MPs) and ULBP1+ T-lymphocyte MPs are linked to acute myocardial infarction (AMI) and its severity. These biomarkers may indicate vulnerable plaques contributing to AMI.

Area of Science:

  • Cardiovascular Biology
  • Immunology
  • Biomarker Discovery

Background:

  • Atherosclerosis is an inflammatory vascular disease leading to coronary artery disease and acute myocardial infarction (AMI).
  • UL16-binding proteins (ULBPs), NKG2D ligands, are expressed on stressed cells and can be released as microparticles (MPs).
  • ULBP1-positive MPs (ULBP1+ MPs) may indicate cellular stress and inflammation in AMI.

Purpose of the Study:

  • To investigate the association between ULBP1+ MPs and the presence of AMI.
  • To determine if ULBP1+ MPs correlate with the severity of AMI, specifically ST-segment elevation myocardial infarction (STEMI) versus non-STEMI (NSTEMI).

Main Methods:

  • Flow cytometry was used to measure ULBP1+ MPs and ULBP1+ T-lymphocyte MPs (ULBP1+ TMPs) in 58 AMI patients and 45 controls.
  • Analysis included assessing the association of MP levels with AMI diagnosis and severity.

Main Results:

  • ULBP1+ MP and ULBP1+ TMP levels were significantly higher in AMI patients compared to controls.
  • Elevated ULBP1+ MPs (OR=4.3) and ULBP1+ TMPs (OR=5.8) were independent risk factors for AMI.
  • ULBP1+ TMP levels were significantly higher in STEMI patients, independently associated with STEMI (OR=3.9).

Conclusions:

  • Increased levels of ULBP1+ MPs and ULBP1+ TMPs are associated with AMI and its severity.
  • These microparticles may serve as potential biomarkers for vulnerable plaques in patients with AMI.
  • ULBP1+ TMPs show promise in differentiating STEMI from NSTEMI.
Abstract

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