The Role of PPAR-gamma in Macrophage Differentiation and Cholesterol Uptake

Overview

Journal Nat Med

Specialties General Medicine
Molecular Biology

Date 2001 Jan 3

PMID 11135614

Citations 152

Authors

K J Moore

E D Rosen

M L Fitzgerald

F RANDOW

L P Andersson

D Altshuler

D S Milstone

R M Mortensen

B M Spiegelman

M W Freeman

Affiliations

Soon will be listed here.

Abstract

Peroxisome proliferator-activated receptor-gamma (PPAR-gamma), the transcription factor target of the anti-diabetic thiazolidinedione (TZD) drugs, is reported to mediate macrophage differentiation and inflammatory responses. Using PPAR-gamma-deficient stem cells, we demonstrate that PPAR-gamma is neither essential for myeloid development, nor for such mature macrophage functions as phagocytosis and inflammatory cytokine production. PPAR-gamma is required for basal expression of CD36, but not for expression of the other major scavenger receptor responsible for uptake of modified lipoproteins, SR-A. In wild-type macrophages, TZD treatment divergently regulated CD36 and class A macrophage-scavenger receptor expression and failed to induce significant cellular cholesterol accumulation, indicating that TZDs may not exacerbate macrophage foam-cell formation.

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