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Molecular and Cellular Biology, April 2002, p. 2607-2619, Vol. 22, No. 8
0270-7306/02/$04.00+0     DOI: 10.1128/MCB.22.8.2607-2619.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Conditional Disruption of the Peroxisome Proliferator-Activated Receptor {gamma} Gene in Mice Results in Lowered Expression of ABCA1, ABCG1, and apoE in Macrophages and Reduced Cholesterol Efflux

Taro E. Akiyama,1 Shuichi Sakai,1,{dagger} Gilles Lambert,2 Christopher J. Nicol,1 Kimihiko Matsusue,1 Satish Pimprale,1,{ddagger} Ying-Hue Lee,1,§ Mercedes Ricote,3 Christopher K. Glass,3 H. Bryan Brewer, Jr.,2 and Frank J. Gonzalez1*

Laboratory of Metabolism, Division of Basic Sciences, National Cancer Institute,1 Molecular Disease Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892,2 Department of Cellular and Molecular Medicine, University of California, San Diego, La Jolla, California 920933

Received 3 July 2001/ Returned for modification 21 September 2001/ Accepted 3 January 2002

Disruption of the peroxisome proliferator-activated receptor {gamma} (PPAR{gamma}) gene causes embryonic lethality due to placental dysfunction. To circumvent this, a PPAR{gamma} conditional gene knockout mouse was produced by using the Cre-loxP system. The targeted allele, containing loxP sites flanking exon 2 of the PPAR{gamma} gene, was crossed into a transgenic mouse line expressing Cre recombinase under the control of the alpha/beta interferon-inducible (MX) promoter. Induction of the MX promoter by pIpC resulted in nearly complete deletion of the targeted exon, a corresponding loss of full-length PPAR{gamma} mRNA transcript and protein, and marked reductions in basal and troglitazone-stimulated expression of the genes encoding lipoprotein lipase, CD36, LXR{alpha}, and ABCG1 in thioglycolate-elicited peritoneal macrophages. Reductions in the basal levels of apolipoprotein E (apoE) mRNA in macrophages and apoE protein in total plasma and high-density lipoprotein (HDL) were also observed in pIpC-treated PPAR{gamma}-MXCre+ mice. Basal cholesterol efflux from cholesterol-loaded macrophages to HDL was significantly reduced after disruption of the PPAR{gamma} gene. Troglitazone selectively inhibited ABCA1 expression (while rosiglitazone, ciglitazone, and pioglitazone had little effect) and cholesterol efflux in both PPAR{gamma}-deficient and control macrophages, indicating that this drug can exert paradoxical effects on cholesterol homeostasis that are independent of PPAR{gamma}. Together, these data indicate that PPAR{gamma} plays a critical role in the regulation of cholesterol homeostasis by controlling the expression of a network of genes that mediate cholesterol efflux from cells and its transport in plasma.

* Corresponding author. Mailing address: Bldg. 37, Rm. 3E-24, National Institutes of Health, Bethesda, MD 20892. Phone: (301) 496-9067. Fax: (301) 496-8419. E-mail: fjgonz{at}helix.nih.gov.

{dagger} Present address: Fuji Gotemba Research Labs, Chugai Pharmaceutical Co., Ltd., Shizuoda 412-8513, Japan.

{ddagger} Gentest Corporation, Woburn, MA 01801.

§ Present address: Institute of Molecular Biology, Academia Sinica, Taipei 115, Taiwan.

Molecular and Cellular Biology, April 2002, p. 2607-2619, Vol. 22, No. 8
0022-538X/02/$04.00+0     DOI: 10.1128/MCB.22.8.2607-2619.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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