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Published on: October 17, 2017
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.
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.
Abstract:
Atherosclerosis is a complex disease in which vessels develop plaques comprising dysfunctional endothelium, monocyte derived lipid laden foam cells and activated lymphocytes. Considering that humans and animal models of the disease develop quite distinct plaques, we used human plaques to search for proteins that could be used as markers of human atheromas. Phage display peptide libraries were probed to fresh human carotid plaques, and a bound phage homologous to plexin B1, a high affinity receptor for CD100, was identified. CD100 is a member of the semaphorin family expressed by most hematopoietic cells and particularly by activated T cells. CD100 expression was analyzed in human plaques and normal samples. CD100 mRNA and protein were analyzed in cultured monocytes, macrophages and foam cells. The effects of CD100 in oxLDL-induced foam cell formation and in CD36 mRNA abundance were evaluated. Human atherosclerotic plaques showed strong labeling of CD100/SEMA4D. CD100 expression was further demonstrated in peripheral blood monocytes and in in vitro differentiated macrophages and foam cells, with diminished CD100 transcript along the differentiation of these cells. Incubation of macrophages with CD100 led to a reduction in oxLDL-induced foam cell formation probably through a decrease of CD36 expression, suggesting for the first time an atheroprotective role for CD100 in the human disease. Given its differential expression in the numerous foam cells and macrophages of the plaques and its capacity to decrease oxLDL engulfment by macrophages we propose that CD100 may have a role in atherosclerotic plaque development, and may possibly be employed in targeted treatments of these atheromas.
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