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Originally published In Press as doi:10.1074/jbc.M011488200 on February 28, 2001

J. Biol. Chem., Vol. 276, Issue 24, 20989-20998, June 15, 2001
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Synergistic Transcriptional Activation of Human Acyl-coenzyme A: Cholesterol Acyltransterase-1 Gene by Interferon-gamma and All-trans-Retinoic Acid THP-1 Cells*

Jin-Bo YangDagger , Zhi-Jun DuanDagger , Wei YaoDagger , Oneil Lee, Li YangDagger , Xin-Ying YangDagger , Xia SunDagger , Catherine C. Y. Chang§, Ta-Yuan Chang§, and Bo-Liang LiDagger ||

From the Dagger  Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China and the § Department of Biochemistry, Dartmouth Medical School, Hanover, New Hampshire 03755

Acyl-coenzyme A:cholesterol acyltransferase (ACAT) is an intracellular enzyme involved in cellular cholesterol homeostasis and in atherosclerotic foam cell formation. Human ACAT-1 gene contains two promoters (P1 and P7), each located in a different chromosome (1 and 7) (Li, B. L., Li, X. L., Duan, Z. J., Lee, O., Lin, S., Ma, Z. M., Chang, C. C., Yang, X. Y., Park, J. P., Mohandas, T. K., Noll, W., Chan, L., and Chang, T. Y. (1999) J. Biol Chem. 274, 11060-11071). Interferon-gamma (IFN-gamma ), a cytokine that exerts many pro-atherosclerotic effects in vivo, causes up-regulation of ACAT-1 mRNA in human blood monocyte-derived macrophages and macrophage-like cells but not in other cell types. To examine the molecular nature of this observation, we identified within the ACAT-1 P1 promoter a 159-base pair core region. This region contains 4 Sp1 elements and an IFN-gamma activated sequence (GAS) that overlaps with the second Sp1 element. In the monocytic cell line THP-1 cell, the combination of IFN-gamma and all-trans-retinoic acid (a known differentiation agent) enhances the ACAT-1 P1 promoter but not the P7 promoter. Additional experiments showed that all-trans-retinoic acid causes large induction of the transcription factor STAT1, while IFN-gamma causes activation of STAT1 such that it binds to the GAS/Sp1 site in the ACAT-1 P1 promoter. Our work provides a molecular mechanism to account for the effect of IFN-gamma in causing transcriptional activation of ACAT-1 in macrophage-like cells.

* This work was supported by National Natural Scientific Foundation of China Grant 39425005 (to B. L. L.), Shanghai Science and Technology Commission Grant 97XD14022 (to B. L. L.), and National Institutes of Health Grant HL 36709 (to T. Y. C.).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 corresponding may be addressed: Dept. of Biochemistry, Dartmouth Medical School, Hanover, NH. Tel.: 603-650-1622; Fax: 603-650-1483; E-mail: Ta.Yuan.Chang@Dartmouth.EDU.

|| To whom correspondence may be addressed: Institute of Biochemistry and Cell Biology, 320 Yue-Yang Road, Shanghai 200031, China. Tel.: 86-21-6474-7035; Fax: 86-21-6433-8357; E-mail:boliang@server.shcnc.ac.cn.

Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.
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