The role of PPAR-γ in macrophage differentiation and cholesterol uptake

被引：442

作者：

Moore, KJ

Rosen, ED

Fitzgerald, ML

Randow, F

Andersson, LP

Altshuler, D

Milstone, DS

Mortensen, RM

Spiegelman, BM

Freeman, MW ^{[1
]}

机构：

[1] Massachusetts Gen Hosp, Dept Med, Lipid Metab Unit, Boston, MA 02114 USA

[2] Harvard Univ, Sch Med, Boston, MA 02115 USA

[3] Dana Farber Canc Inst, Dept Cell Biol, Boston, MA 02115 USA

[4] Massachusetts Gen Hosp, Dept Mol Biol, Boston, MA 02114 USA

[5] MIT, Whitehead Inst Biomed Res, Ctr Genome Res, Cambridge, MA 02139 USA

[6] Brigham & Womens Hosp, Dept Pathol, Div Vasc Res, Boston, MA 02115 USA

[7] Univ Michigan, Dept Physiol, Div Endocrine, Ann Arbor, MI 48109 USA

来源：

NATURE MEDICINE | 2001年 / 7卷 / 01期

关键词：

D O I：

10.1038/83328

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

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.

引用

页码：41 / 47

页数：7

共 47 条

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