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Related Experiment Video

Updated: Jul 16, 2026

Investigation of Macrophage Polarization Using Bone Marrow Derived Macrophages

Investigation of Macrophage Polarization Using Bone Marrow Derived Macrophages

Published on: June 23, 2013

PPARalpha agonists suppress osteopontin expression in macrophages and decrease plasma levels in patients with type 2

Takafumi Nakamachi¹, Takashi Nomiyama, Florence Gizard

¹Division of Endocrinology and Molecular Medicine, Department of Internal Medicine, University of Kentucky College of Medicine, Lexington, Kentucky 40536-0200, USA.

|March 16, 2007

Summary

Peroxisome proliferator-activated receptor (PPAR)alpha agonists reduce osteopontin (OPN) in macrophages and patients with type 2 diabetes. This suggests PPARalpha ligands may lower cardiovascular disease risk by inhibiting inflammatory markers.

Related Experiment Videos

Last Updated: Jul 16, 2026

Investigation of Macrophage Polarization Using Bone Marrow Derived Macrophages

Investigation of Macrophage Polarization Using Bone Marrow Derived Macrophages

Published on: June 23, 2013

Area of Science:

Cardiovascular Research
Molecular Biology
Immunology

Background:

Osteopontin (OPN) is a pro-inflammatory cytokine linked to atherosclerosis.
Peroxisome proliferator-activated receptor (PPAR)alpha agonists, like fibrates, have anti-inflammatory effects and treat dyslipidemia in type 2 diabetes patients.
Fibrates are commonly prescribed for patients with type 2 diabetes and high cardiovascular disease risk.

Purpose of the Study:

To investigate how PPARalpha agonists regulate OPN expression in macrophages.
To determine the impact of fibrate treatment on plasma OPN levels in type 2 diabetes patients.

Main Methods:

Human macrophages were treated with PPARalpha ligands (bezafibrate, WY14643).
OPN promoter activity, AP-1 binding, and c-Fos/c-Jun expression were analyzed.
Chromatin immunoprecipitation assays were performed.
PPARalpha-deficient macrophages were used to confirm receptor-mediated effects.
Type 2 diabetes patients received bezafibrate, and plasma OPN levels were measured.

Main Results:

PPARalpha ligands inhibited OPN expression and promoter activity in macrophages.
This inhibition was mediated by negative cross-talk with AP-1 transcription factors (c-Fos, c-Jun).
The effect was dependent on PPARalpha receptor presence.
Bezafibrate treatment significantly reduced plasma OPN levels in type 2 diabetes patients.

Conclusions:

PPARalpha agonists suppress OPN expression in macrophages via a PPARalpha-dependent, AP-1-mediated mechanism.
Fibrate therapy may reduce cardiovascular disease risk by lowering OPN, an early inflammatory marker.