A Novel Liver X Receptor Agonist Establishes Species Differences in the Regulation of Cholesterol 7α-Hydroxylase (CYP7a) (original) (raw)

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John G. Menke ,

1Molecular Endocrinology (J.G.M., K.L.M., N.S.H., L.J.K., P.X., G.Z., D.E.M.) at Merck & Co., Rahway, New Jersey 07065

*Address all correspondence and requests for reprints to: John Menke, Merck Research Laboratories, Department of Molecular Endocrinology, RY80W-207, 126 East Lincoln Avenue, Rahway, New Jersey 07065.

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Karen L. Macnaul ,

1Molecular Endocrinology (J.G.M., K.L.M., N.S.H., L.J.K., P.X., G.Z., D.E.M.) at Merck & Co., Rahway, New Jersey 07065

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Nancy S. Hayes ,

1Molecular Endocrinology (J.G.M., K.L.M., N.S.H., L.J.K., P.X., G.Z., D.E.M.) at Merck & Co., Rahway, New Jersey 07065

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Joanne Baffic ,

2Atherosclerosis and Endocrinology (J.B., Y.-S.C., M.-H.L., S.D.W., C.P.S.) at Merck & Co., Rahway, New Jersey 07065

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Yu-Sheng Chao ,

2Atherosclerosis and Endocrinology (J.B., Y.-S.C., M.-H.L., S.D.W., C.P.S.) at Merck & Co., Rahway, New Jersey 07065

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Alex Elbrecht ,

3Bioinformatics (A.E.) at Merck & Co., Rahway, New Jersey 07065

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Linda J. Kelly ,

1Molecular Endocrinology (J.G.M., K.L.M., N.S.H., L.J.K., P.X., G.Z., D.E.M.) at Merck & Co., Rahway, New Jersey 07065

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My-Hanh Lam ,

2Atherosclerosis and Endocrinology (J.B., Y.-S.C., M.-H.L., S.D.W., C.P.S.) at Merck & Co., Rahway, New Jersey 07065

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Azriel Schmidt ,

5Bone Biology (A.S.) at Merck & Co., West Point, Pennsylvania 19486

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Soumya Sahoo

4Medicinal Chemistry (S.S.) at Merck & Co., Rahway, New Jersey 07065

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Received:

06 November 2001

Cite

John G. Menke, Karen L. Macnaul, Nancy S. Hayes, Joanne Baffic, Yu-Sheng Chao, Alex Elbrecht, Linda J. Kelly, My-Hanh Lam, Azriel Schmidt, Soumya Sahoo, Jianhua Wang, Samuel D. Wright, Patrick Xin, Gaochao Zhou, David E. Moller, Carl P. Sparrow, A Novel Liver X Receptor Agonist Establishes Species Differences in the Regulation of Cholesterol 7α-Hydroxylase (CYP7a), Endocrinology, Volume 143, Issue 7, 1 July 2002, Pages 2548–2558, https://doi.org/10.1210/endo.143.7.8907
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Abstract

The liver X receptors, LXRα and LXRβ, are members of the nuclear receptor superfamily. Originally identified as orphans, both receptor subtypes have since been shown to be activated by naturally occurring oxysterols. LXRα knockout mice fail to regulate cyp7a mRNA levels upon cholesterol feeding, implicating the role of this receptor in cholesterol homeostasis. LXR activation also induces the expression of the lipid pump involved in cholesterol efflux, the gene encoding ATP binding cassette protein A1 (ABCA1). Therefore, LXR is believed to be a sensor of cholesterol levels and a potential therapeutic target for atherosclerosis. Here we describe a synthetic molecule named F3MethylAA [3-chloro-4-(3-(7-propyl-3-trifluoromethyl-6-(4,5)-isoxazolyl)propylthio)-phenyl acetic acid] that is more potent than 22(R)-hydroxycholesterol in LXR in vitro assays. F3MethylAA is capable not only of inducing ABCA1 mRNA levels, but also increasing cholesterol efflux from THP-1 macrophages. In rat hepatocytes, F3MethylAA induced cyp7a mRNA, confirming conclusions from the knockout mouse studies. Furthermore, in rat in vivo studies, F3MethylAA induced liver cyp7a mRNA and enzyme activity. A critical species difference is also reported in that neither F3MethylAA nor 22(R)-hydroxycholesterol induced cyp7a in human primary hepatocytes. However, other LXR target genes, ABCA1, ABCG1, and SREBP1, were regulated.

Copyright © 2002 by The Endocrine Society

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