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Aspirin increases CD36, SR-BI, and ABCA1 expression in human THP-1 macrophages
Marisa Viñals1, Ignacio Bermúdez, Gemma Llaverias
1Unitat de Farmacologia, Facultat de Farmacia, Universitat de Barcelona, Nucli Universitari de Pedralbes, E-08028 Barcelona, Spain. mvinals@lloguerspous.com
Insights
Aspirin increases CD36 expression in macrophages through a prostaglandin E2 (PGE2)-dependent pathway, involving EP2/EP4 receptors. This study also observed aspirin-induced expression of SR-BI and ABCA1.
Area of Science:
- Immunology
- Cell Biology
- Biochemistry
Background:
- CD36 receptor expression rises during monocyte to macrophage differentiation.
- CD36 is crucial for apoptotic cell phagocytosis and foam cell formation in atherosclerosis.
- PPARgamma ligands increase CD36 and inhibit cyclooxygenase in macrophages.
Purpose of the Study:
- Investigate if reduced prostaglandin production affects macrophage CD36 expression.
- Elucidate the potential mechanism behind CD36 modulation by prostaglandins.
Main Methods:
- THP-1 cells differentiated into macrophages were treated with aspirin (ASA) alone or with various prostaglandin E2 (PGE2) analogs.
- CD36 expression was quantified using flow cytometry.
- PPARgamma antagonists and cyclooxygenase inhibitors were used to explore mechanisms.
Main Results:
- Aspirin significantly induced CD36 expression in macrophages.
- PGE2 and PGE1 alcohol fully blocked aspirin-induced CD36 expression, while butaprost partially reduced it.
- Aspirin also upregulated scavenger receptor class B type I (SR-BI) and ATP-binding cassette transporter A1 (ABCA1) expression.
Conclusions:
- Aspirin enhances CD36 expression in THP-1 macrophages via a PGE2-dependent mechanism.
- EP2 and EP4 prostaglandin E2 receptor subtypes are implicated in CD36 modulation by aspirin.
- Aspirin treatment also induces SR-BI and ABCA1 expression in macrophages.
Objective:
CD36 is a receptor, whose expression increases during the differentiation of monocytes to macrophages, playing a key role in the phagocytosis of apoptotic cells and in the formation of foam cells during atherosclerosis. Recently, it has been described that ligands of PPARgamma induce CD36 expression and inhibit cyclooxygenase expression in macrophages. Our aim was to study whether the reduction of endogenous prostaglandin production could modify CD36 expression in macrophages and to outline the potential mechanism.
Methods And Results:
CD36 expression was measured by flow cytometry in THP-1 cells differentiated to macrophages that had been incubated with aspirin (ASA) alone or in combination with PGE(2), sulprostone (EP1/EP3 agonist), butaprost (EP2 agonist,) and PGE1 alcohol (EP2/EP4 agonist). Aspirin induced CD36 expression. Only PGE(2) and PGE1 alcohol completely abolished CD36 induction by aspirin, whereas butaprost strongly reduced it. BADGE (a PPARgamma antagonist) or diclofenac (a PPARgamma antagonist and a cyclooxygenase inhibitor) in aspirin-incubated cells did not reduce CD36 induction. On the other hand, aspirin also induced the expression of SR-BI and ABCA1, an HDL receptor and an HDL formation-related protein, respectively.
Conclusions:
Aspirin produces an increase of CD36 expression in THP-1 macrophages by a PGE(2)-dependent mechanism. The PGE(2) receptors implicated in CD36 modulation by ASA are the EP2/EP4 subtypes. Further, we provide evidence of SR-BI and ABCA1 induction by aspirin treatment.
