Retinoic Acid Receptor-Mediated Induction of ABCA1 in Macrophages

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Published in	Molecular and Cellular Biology Vol. 23; no. 21; pp. 7756 - 7766
Main Authors	Costet, Philippe, Lalanne, Florent, Gerbod-Giannone, Marie C, Molina, Jennifer R, Fu, Xuan, Lund, Erik G, Gudas, Lorraine J, Tall, Alan R
Format	Journal Article
Language	English
Published	United States American Society for Microbiology 01.11.2003 Taylor & Francis
Subjects	Animals ATP Binding Cassette Transporter 1 ATP-Binding Cassette Transporters - genetics ATP-Binding Cassette Transporters - metabolism Biological Transport - physiology CCAAT-Enhancer-Binding Proteins - genetics CCAAT-Enhancer-Binding Proteins - metabolism Cells, Cultured Cholesterol - metabolism DNA-Binding Proteins - genetics DNA-Binding Proteins - metabolism Gene Expression Gene Expression Regulation Humans Liver - metabolism Liver X Receptors Macrophages - cytology Macrophages - physiology Male Mice Mice, Inbred C57BL Mice, Knockout Orphan Nuclear Receptors Promoter Regions, Genetic Receptors, Cytoplasmic and Nuclear - genetics Receptors, Cytoplasmic and Nuclear - metabolism Receptors, Retinoic Acid - genetics Receptors, Retinoic Acid - metabolism Sterol Regulatory Element Binding Protein 1 Transcription Factors Tretinoin - metabolism
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Abstract	Article Usage Stats Services MCB Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley Reddit StumbleUpon Twitter current issue Spotlights in the Current Issue MCB About MCB Subscribers Authors Reviewers Advertisers Inquiries from the Press Permissions & Commercial Reprints ASM Journals Public Access Policy MCB RSS Feeds 1752 N Street N.W. • Washington DC 20036 202.737.3600 • 202.942.9355 fax • journals@asmusa.org Print ISSN: 0270-7306 Online ISSN: 1098-5549 Copyright © 2014 by the American Society for Microbiology. For an alternate route to MCB .asm.org, visit: MCB
AbstractList	ABCA1, the mutant molecule in Tangier Disease, mediates efflux of cellular cholesterol to apoA-I and is induced by liver X receptor (LXR)/retinoid X receptor (RXR) transcription factors. Retinoic acid receptor (RAR) activators (all- trans -retinoic acid [ATRA] and TTNPB) were found to increase ATP-binding cassette transporter 1 (ABCA1) mRNA and protein in macrophages. In cellular cotransfection assays, RARγ/RXR activated the human ABCA1 promoter, via the same direct repeat 4 (DR4) promoter element as LXR/RXR. Chromatin immunoprecipitation analysis in macrophages confirmed the binding of RARγ/RXR to the ABCA1 promoter DR4 element in the presence of ATRA, with weaker binding of RARα/RXR, and no binding of RARβ/RXR. However, in macrophages from RARγ −/− mice, TTNPB still induced ABCA1, in association with marked upregulation of RARα, suggesting that high levels of RARα can compensate for the absence of RARγ. Dose-response experiments with ATRA in mouse primary macrophages showed that other LXR target genes were weakly induced (ABCG1 and SREBP-1c) or not induced (apoE and LXRα). The more specific RAR activator TTNPB did not induce SREBP-1c in mouse primary macrophages or liver. These studies indicate a direct role of RARγ/RXR in induction of macrophage ABCA1. ABCA1, the mutant molecule in Tangier Disease, mediates efflux of cellular cholesterol to apoA-I and is induced by liver X receptor (LXR)/retinoid X receptor (RXR) transcription factors. Retinoic acid receptor (RAR) activators (all-trans-retinoic acid [ATRA] and TTNPB) were found to increase ATP-binding cassette transporter 1 (ABCA1) mRNA and protein in macrophages. In cellular cotransfection assays, RARγ/RXR activated the human ABCA1 promoter, via the same direct repeat 4 (DR4) promoter element as LXR/RXR. Chromatin immunoprecipitation analysis in macrophages confirmed the binding of RARγ/RXR to the ABCA1 promoter DR4 element in the presence of ATRA, with weaker binding of RARα/RXR, and no binding of RARβ/RXR. However, in macrophages from RARγ −/− mice, TTNPB still induced ABCA1, in association with marked upregulation of RARα, suggesting that high levels of RARα can compensate for the absence of RARγ. Dose-response experiments with ATRA in mouse primary macrophages showed that other LXR target genes were weakly induced (ABCG1 and SREBP-1c) or not induced (apoE and LXRα). The more specific RAR activator TTNPB did not induce SREBP-1c in mouse primary macrophages or liver. These studies indicate a direct role of RARγ/RXR in induction of macrophage ABCA1. Article Usage Stats Services MCB Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley Reddit StumbleUpon Twitter current issue Spotlights in the Current Issue MCB About MCB Subscribers Authors Reviewers Advertisers Inquiries from the Press Permissions & Commercial Reprints ASM Journals Public Access Policy MCB RSS Feeds 1752 N Street N.W. • Washington DC 20036 202.737.3600 • 202.942.9355 fax • journals@asmusa.org Print ISSN: 0270-7306 Online ISSN: 1098-5549 Copyright © 2014 by the American Society for Microbiology. For an alternate route to MCB .asm.org, visit: MCB ABCA1, the mutant molecule in Tangier Disease, mediates efflux of cellular cholesterol to apoA-I and is induced by liver X receptor (LXR)/retinoid X receptor (RXR) transcription factors. Retinoic acid receptor (RAR) activators (all-trans-retinoic acid [ATRA] and TTNPB) were found to increase ATP-binding cassette transporter 1 (ABCA1) mRNA and protein in macrophages. In cellular cotransfection assays, RARgamma/RXR activated the human ABCA1 promoter, via the same direct repeat 4 (DR4) promoter element as LXR/RXR. Chromatin immunoprecipitation analysis in macrophages confirmed the binding of RARgamma/RXR to the ABCA1 promoter DR4 element in the presence of ATRA, with weaker binding of RARalpha/RXR, and no binding of RARbeta/RXR. However, in macrophages from RARgamma(-/-) mice, TTNPB still induced ABCA1, in association with marked upregulation of RARalpha, suggesting that high levels of RARalpha can compensate for the absence of RARgamma. Dose-response experiments with ATRA in mouse primary macrophages showed that other LXR target genes were weakly induced (ABCG1 and SREBP-1c) or not induced (apoE and LXRalpha). The more specific RAR activator TTNPB did not induce SREBP-1c in mouse primary macrophages or liver. These studies indicate a direct role of RARgamma/RXR in induction of macrophage ABCA1. ABCA1, the mutant molecule in Tangier Disease, mediates efflux of cellular cholesterol to apoA-I and is induced by liver X receptor (LXR)/retinoid X receptor (RXR) transcription factors. Retinoic acid receptor (RAR) activators (all-trans-retinoic acid (ATRA) and TTNPB) were found to increase ATP- binding cassette transporter 1 (ABCA1) mRNA and protein in macrophages. In cellular cotransfection assays, RAR gamma /RXR activated the human ABCA1 promoter, via the same direct repeat 4 (DR4) promoter element as LXR/RXR. Chromatin immunoprecipitation analysis in macrophages confirmed the binding of RAR gamma /RXR to the ABCA1 promoter DR4 element in the presence of ATRA, with weaker binding of RAR alpha /RXR, and no binding of RAR beta /RXR. However, in macrophages from RAR gamma super(-/-) mice, TTNPB still induced ABCA1, in association with marked upregulation of RAR alpha , suggesting that high levels of RAR alpha can compensate for the absence of RAR gamma . Dose-response experiments with ATRA in mouse primary macrophages showed that other LXR target genes were weakly induced (ABCG1 and SREBP-1c) or not induced (apoE and LXR alpha ). The more specific RAR activator TTNPB did not induce SREBP-1c in mouse primary macrophages or liver. These studies indicate a direct role of RAR gamma /RXR in induction of macrophage ABCA1.
Author	Marie C. Gerbod-Giannone Xuan Fu Jennifer R. Molina Florent Lalanne Alan R. Tall Philippe Costet Lorraine J. Gudas Erik G. Lund
AuthorAffiliation	Division of Molecular Medicine, Department of Medicine, Columbia University, New York, New York 10032, 1 Department of Atherosclerosis and Endocrinology, Merck Research Laboratories, Rahway, New Jersey 07065, 2 Department of Pharmacology, Weill Medical College of Cornell University, New York, New York 10021 3
AuthorAffiliation_xml	– name: Division of Molecular Medicine, Department of Medicine, Columbia University, New York, New York 10032, 1 Department of Atherosclerosis and Endocrinology, Merck Research Laboratories, Rahway, New Jersey 07065, 2 Department of Pharmacology, Weill Medical College of Cornell University, New York, New York 10021 3
Author_xml	– sequence: 1 givenname: Philippe surname: Costet fullname: Costet, Philippe organization: Division of Molecular Medicine, Department of Medicine, Columbia University, New York, New York 10032, USA – sequence: 2 givenname: Florent surname: Lalanne fullname: Lalanne, Florent – sequence: 3 givenname: Marie C surname: Gerbod-Giannone fullname: Gerbod-Giannone, Marie C – sequence: 4 givenname: Jennifer R surname: Molina fullname: Molina, Jennifer R – sequence: 5 givenname: Xuan surname: Fu fullname: Fu, Xuan – sequence: 6 givenname: Erik G surname: Lund fullname: Lund, Erik G – sequence: 7 givenname: Lorraine J surname: Gudas fullname: Gudas, Lorraine J – sequence: 8 givenname: Alan R surname: Tall fullname: Tall, Alan R
BackLink	https://www.ncbi.nlm.nih.gov/pubmed/14560020$$D View this record in MEDLINE/PubMed
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Snippet	Article Usage Stats Services MCB Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley... ABCA1, the mutant molecule in Tangier Disease, mediates efflux of cellular cholesterol to apoA-I and is induced by liver X receptor (LXR)/retinoid X receptor...
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SubjectTerms	Animals ATP Binding Cassette Transporter 1 ATP-Binding Cassette Transporters - genetics ATP-Binding Cassette Transporters - metabolism Biological Transport - physiology CCAAT-Enhancer-Binding Proteins - genetics CCAAT-Enhancer-Binding Proteins - metabolism Cells, Cultured Cholesterol - metabolism DNA-Binding Proteins - genetics DNA-Binding Proteins - metabolism Gene Expression Gene Expression Regulation Humans Liver - metabolism Liver X Receptors Macrophages - cytology Macrophages - physiology Male Mice Mice, Inbred C57BL Mice, Knockout Orphan Nuclear Receptors Promoter Regions, Genetic Receptors, Cytoplasmic and Nuclear - genetics Receptors, Cytoplasmic and Nuclear - metabolism Receptors, Retinoic Acid - genetics Receptors, Retinoic Acid - metabolism Sterol Regulatory Element Binding Protein 1 Transcription Factors Tretinoin - metabolism
Title	Retinoic Acid Receptor-Mediated Induction of ABCA1 in Macrophages
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