Phage display identification of CD100 in human atherosclerotic plaque macrophages and foam cells

Maria Carolina Aquino Luque1, Paulo Sampaio Gutierrez, Victor Debbas

  • 1Heart Institute of São Paulo (InCor), HC-FMUSP, São Paulo, São Paulo, Brazil ; Clinical Immunology and Allergy, Department of Clinical Medicine, University of São Paulo Medical School - HC-FMUSP, São Paulo, São Paulo, Brazil.

Plos One
|October 8, 2013
PubMed

Insights

CD100, a protein found in human atherosclerotic plaques, may protect against atherosclerosis by reducing foam cell formation. This discovery suggests CD100 could be a target for treating human atheromas.

Area of Science:

  • Cardiovascular Biology
  • Immunology
  • Molecular Medicine

Background:

  • Atherosclerosis involves complex plaque development with distinct human and animal models.
  • Identifying human-specific markers is crucial for understanding atheroma formation.

Purpose of the Study:

  • To identify novel protein markers in human atherosclerotic plaques.
  • To investigate the role of CD100 (semaphorin 4D) in human atherosclerosis.

Main Methods:

  • Phage display libraries were used to screen human carotid plaques.
  • CD100 expression was analyzed in plaques, blood cells, and differentiated macrophages.
  • The impact of CD100 on oxidized LDL-induced foam cell formation and CD36 expression was evaluated.

Main Results:

  • A phage homologous to plexin B1, a CD100 receptor, was identified.
  • Human atherosclerotic plaques showed significant CD100/SEMA4D labeling.
  • CD100 reduced oxidized LDL uptake by macrophages, likely via decreased CD36 expression.

Conclusions:

  • CD100 is expressed in human atherosclerotic plaques and associated cells.
  • CD100 demonstrates a potential atheroprotective role by inhibiting foam cell formation.
  • CD100 may serve as a therapeutic target for atherosclerotic disease.