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Originally published In Press as doi:10.1074/jbc.M200875200 on February 14, 2002

J. Biol. Chem., Vol. 277, Issue 19, 16913-16919, May 10, 2002
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Peroxisome Proliferator-activated Receptor gamma  Agonists Inhibit HIV-1 Replication in Macrophages by Transcriptional and Post-transcriptional Effects*

Michael M. HayesDagger , Brian R. Lane§, Steven R. King, David M. Markovitz§||, and Michael J. CoffeyDagger **

From the Dagger  Divisions of Pulmonary and Critical Care Medicine,  Rheumatology, and || Infectious Diseases and the § Graduate Program in Cellular and Molecular Biology, University of Michigan Medical Center, Ann Arbor, Michigan 48109

Previous studies have demonstrated that cyclopentenone prostaglandins (cyPG) inhibit human immunodeficiency virus type 1 (HIV-1) replication in various cell types. We investigated the role of PG in the replication of HIV-1 in primary macrophages. The cyPG, PGA1 and PGA2, inhibited HIV-1 replication in acutely infected human monocyte-derived macrophages (MDM). Because PGA1 and PGA2 have previously been shown to be peroxisome proliferator-activated receptor gamma  (PPARgamma ) agonists, we examined the effect of synthetic PPARgamma agonists on HIV replication. The PPARgamma agonist ciglitazone inhibited HIV-1 replication in a dose-dependent manner in acutely infected human MDM. In addition, cyPG and ciglitazone reduced HIV replication in latently infected and viral entry-independent U1 cells, suggesting an effect at the level of HIV gene expression. Ciglitazone also suppressed HIV-1 mRNA levels as measured by reverse transcriptase PCR, in parallel with the decrease in reverse transcriptase activity. Co-transfection of PPARgamma wild type vectors and treatment with PPARgamma agonists inhibited HIV-1 promoter activity in U937 cells. Activation of PPARgamma also decreased HIV-1 mRNA stability following actinomycin D treatment. In summary, our experimental findings implicate PPARgamma as an important factor in the suppression of HIV-1 gene expression in MDM by cyPG. Thus natural and synthetic PPARgamma agonists may play a role in controlling HIV-1 infection in macrophages.

* This work was supported by National Institutes of Health Grants AI36685 (to D. M. M.) and HL57885 (to M. J. C.), the General Clinical Research Center at the University of Michigan (Grant MOI-RR00042), the Medical Scientist Training Program of the University of Michigan (National Institutes of Health Grant NIGMS T32GM07863 to B. R. L.), and funds from the Harvey fellows programs (to B. R. L.).The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

** To whom correspondence should be addressed: University of Michigan Medical Center, 6301 MSRB III, 1150 W. Medical Center Dr., Ann Arbor, MI 48109-0642. Tel.: 734-764-4554; Fax: 734-764-4556; E-mail: coffeym@umich.edu.

Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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