SREBP1 Contributes to Resolution of Pro-inflammatory TLR4 Signaling by Reprogramming Fatty Acid Metabolism

Macrophages play pivotal roles in both the induction and resolution phases of inflammatory processes. Macrophages have been shown to synthesize anti-inflammatory fatty acids in an LXR-dependent manner, but whether the production of these species contributes to the resolution phase of inflammatory re...

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Vydáno v:	Cell metabolism Ročník 25; číslo 2; s. 412
Hlavní autoři:	Oishi, Yumiko, Spann, Nathanael J, Link, Verena M, Muse, Evan D, Strid, Tobias, Edillor, Chantle, Kolar, Matthew J, Matsuzaka, Takashi, Hayakawa, Sumio, Tao, Jenhan, Kaikkonen, Minna U, Carlin, Aaron F, Lam, Michael T, Manabe, Ichiro, Shimano, Hitoshi, Saghatelian, Alan, Glass, Christopher K
Médium:	Journal Article
Jazyk:	angličtina
Vydáno:	United States 07.02.2017
Témata:	Animals Base Sequence Biosynthetic Pathways - drug effects Biosynthetic Pathways - genetics Enhancer Elements, Genetic - genetics Fatty Acids - metabolism Inflammation - genetics Inflammation - pathology Lipid Metabolism - drug effects Lipopolysaccharides - pharmacology Liver X Receptors - metabolism Macrophages - drug effects Macrophages - metabolism Male Mice, Inbred C57BL Phenotype Signal Transduction - drug effects Sterol Regulatory Element Binding Protein 1 - metabolism Time Factors Toll-Like Receptor 4 - metabolism innate immunity unsaturated fatty acids inflammation fatty acid metabolism transcriptional regulation EPA lipid metabolism SREBP1 DHA resolution
ISSN:	1932-7420, 1932-7420
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Abstract	Macrophages play pivotal roles in both the induction and resolution phases of inflammatory processes. Macrophages have been shown to synthesize anti-inflammatory fatty acids in an LXR-dependent manner, but whether the production of these species contributes to the resolution phase of inflammatory responses has not been established. Here, we identify a biphasic program of gene expression that drives production of anti-inflammatory fatty acids 12-24 hr following TLR4 activation and contributes to downregulation of mRNAs encoding pro-inflammatory mediators. Unexpectedly, rather than requiring LXRs, this late program of anti-inflammatory fatty acid biosynthesis is dependent on SREBP1 and results in the uncoupling of NFκB binding from gene activation. In contrast to previously identified roles of SREBP1 in promoting production of IL1β during the induction phase of inflammation, these studies provide evidence that SREBP1 also contributes to the resolution phase of TLR4-induced gene activation by reprogramming macrophage lipid metabolism.
AbstractList	Macrophages play pivotal roles in both the induction and resolution phases of inflammatory processes. Macrophages have been shown to synthesize anti-inflammatory fatty acids in an LXR-dependent manner, but whether the production of these species contributes to the resolution phase of inflammatory responses has not been established. Here, we identify a biphasic program of gene expression that drives production of anti-inflammatory fatty acids 12-24 hr following TLR4 activation and contributes to downregulation of mRNAs encoding pro-inflammatory mediators. Unexpectedly, rather than requiring LXRs, this late program of anti-inflammatory fatty acid biosynthesis is dependent on SREBP1 and results in the uncoupling of NFκB binding from gene activation. In contrast to previously identified roles of SREBP1 in promoting production of IL1β during the induction phase of inflammation, these studies provide evidence that SREBP1 also contributes to the resolution phase of TLR4-induced gene activation by reprogramming macrophage lipid metabolism.Macrophages play pivotal roles in both the induction and resolution phases of inflammatory processes. Macrophages have been shown to synthesize anti-inflammatory fatty acids in an LXR-dependent manner, but whether the production of these species contributes to the resolution phase of inflammatory responses has not been established. Here, we identify a biphasic program of gene expression that drives production of anti-inflammatory fatty acids 12-24 hr following TLR4 activation and contributes to downregulation of mRNAs encoding pro-inflammatory mediators. Unexpectedly, rather than requiring LXRs, this late program of anti-inflammatory fatty acid biosynthesis is dependent on SREBP1 and results in the uncoupling of NFκB binding from gene activation. In contrast to previously identified roles of SREBP1 in promoting production of IL1β during the induction phase of inflammation, these studies provide evidence that SREBP1 also contributes to the resolution phase of TLR4-induced gene activation by reprogramming macrophage lipid metabolism. Macrophages play pivotal roles in both the induction and resolution phases of inflammatory processes. Macrophages have been shown to synthesize anti-inflammatory fatty acids in an LXR-dependent manner, but whether the production of these species contributes to the resolution phase of inflammatory responses has not been established. Here, we identify a biphasic program of gene expression that drives production of anti-inflammatory fatty acids 12-24 hr following TLR4 activation and contributes to downregulation of mRNAs encoding pro-inflammatory mediators. Unexpectedly, rather than requiring LXRs, this late program of anti-inflammatory fatty acid biosynthesis is dependent on SREBP1 and results in the uncoupling of NFκB binding from gene activation. In contrast to previously identified roles of SREBP1 in promoting production of IL1β during the induction phase of inflammation, these studies provide evidence that SREBP1 also contributes to the resolution phase of TLR4-induced gene activation by reprogramming macrophage lipid metabolism.
Author	Kolar, Matthew J Spann, Nathanael J Hayakawa, Sumio Link, Verena M Matsuzaka, Takashi Saghatelian, Alan Oishi, Yumiko Muse, Evan D Glass, Christopher K Kaikkonen, Minna U Shimano, Hitoshi Manabe, Ichiro Tao, Jenhan Lam, Michael T Edillor, Chantle Strid, Tobias Carlin, Aaron F
Author_xml	– sequence: 1 givenname: Yumiko surname: Oishi fullname: Oishi, Yumiko email: yuooishi-circ@umin.ac.jp organization: Department of Cellular and Molecular Medicine, School of Medicine, University of California, San Diego, La Jolla, CA 92093, USA; Department of Cellular and Molecular Medicine, Medical Research Institute, Tokyo Medical and Dental University, Tokyo 113-8510, Japan. Electronic address: yuooishi-circ@umin.ac.jp – sequence: 2 givenname: Nathanael J surname: Spann fullname: Spann, Nathanael J organization: Department of Cellular and Molecular Medicine, School of Medicine, University of California, San Diego, La Jolla, CA 92093, USA – sequence: 3 givenname: Verena M surname: Link fullname: Link, Verena M organization: Department of Cellular and Molecular Medicine, School of Medicine, University of California, San Diego, La Jolla, CA 92093, USA; Department II, Faculty of Biology, Ludwig-Maximilians Universität München, Planegg-Martinsried 82152, Germany – sequence: 4 givenname: Evan D surname: Muse fullname: Muse, Evan D organization: Department of Cellular and Molecular Medicine, School of Medicine, University of California, San Diego, La Jolla, CA 92093, USA; Scripps Translational Science Institute, La Jolla, CA 92037, USA – sequence: 5 givenname: Tobias surname: Strid fullname: Strid, Tobias organization: Department of Cellular and Molecular Medicine, School of Medicine, University of California, San Diego, La Jolla, CA 92093, USA – sequence: 6 givenname: Chantle surname: Edillor fullname: Edillor, Chantle organization: Department of Cellular and Molecular Medicine, School of Medicine, University of California, San Diego, La Jolla, CA 92093, USA – sequence: 7 givenname: Matthew J surname: Kolar fullname: Kolar, Matthew J organization: Salk Institute for Biological Studies, La Jolla, CA 92037, USA – sequence: 8 givenname: Takashi surname: Matsuzaka fullname: Matsuzaka, Takashi organization: Department of Internal Medicine (Endocrinology and Metabolism), Faculty of Medicine, Graduate School of Comprehensive Human Sciences, International Institute for Integrative Sleep Medicine (WPI-IIIS), and Center for Tsukuba Advanced Research Alliance, University of Tsukuba, Ibaraki Prefecture 305-8571, Japan – sequence: 9 givenname: Sumio surname: Hayakawa fullname: Hayakawa, Sumio organization: Department of Cellular and Molecular Medicine, Medical Research Institute, Tokyo Medical and Dental University, Tokyo 113-8510, Japan – sequence: 10 givenname: Jenhan surname: Tao fullname: Tao, Jenhan organization: Department of Cellular and Molecular Medicine, School of Medicine, University of California, San Diego, La Jolla, CA 92093, USA – sequence: 11 givenname: Minna U surname: Kaikkonen fullname: Kaikkonen, Minna U organization: Department of Cellular and Molecular Medicine, School of Medicine, University of California, San Diego, La Jolla, CA 92093, USA; Department of Biotechnology and Molecular Medicine, A.I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, P.O. Box 1627, 70211 Kuopio, Finland – sequence: 12 givenname: Aaron F surname: Carlin fullname: Carlin, Aaron F organization: Department of Cellular and Molecular Medicine, School of Medicine, University of California, San Diego, La Jolla, CA 92093, USA – sequence: 13 givenname: Michael T surname: Lam fullname: Lam, Michael T organization: Department of Cellular and Molecular Medicine, School of Medicine, University of California, San Diego, La Jolla, CA 92093, USA – sequence: 14 givenname: Ichiro surname: Manabe fullname: Manabe, Ichiro organization: Department of Aging Research, Graduate School of Medicine, Chiba University, Chiba 260-8670, Japan – sequence: 15 givenname: Hitoshi surname: Shimano fullname: Shimano, Hitoshi organization: Department of Internal Medicine (Endocrinology and Metabolism), Faculty of Medicine, Graduate School of Comprehensive Human Sciences, International Institute for Integrative Sleep Medicine (WPI-IIIS), and Center for Tsukuba Advanced Research Alliance, University of Tsukuba, Ibaraki Prefecture 305-8571, Japan – sequence: 16 givenname: Alan surname: Saghatelian fullname: Saghatelian, Alan organization: Salk Institute for Biological Studies, La Jolla, CA 92037, USA – sequence: 17 givenname: Christopher K surname: Glass fullname: Glass, Christopher K email: ckg@ucsd.edu organization: Department of Cellular and Molecular Medicine, School of Medicine, University of California, San Diego, La Jolla, CA 92093, USA. Electronic address: ckg@ucsd.edu
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Snippet	Macrophages play pivotal roles in both the induction and resolution phases of inflammatory processes. Macrophages have been shown to synthesize...
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SubjectTerms	Animals Base Sequence Biosynthetic Pathways - drug effects Biosynthetic Pathways - genetics Enhancer Elements, Genetic - genetics Fatty Acids - metabolism Inflammation - genetics Inflammation - pathology Lipid Metabolism - drug effects Lipopolysaccharides - pharmacology Liver X Receptors - metabolism Macrophages - drug effects Macrophages - metabolism Male Mice, Inbred C57BL Phenotype Signal Transduction - drug effects Sterol Regulatory Element Binding Protein 1 - metabolism Time Factors Toll-Like Receptor 4 - metabolism
Title	SREBP1 Contributes to Resolution of Pro-inflammatory TLR4 Signaling by Reprogramming Fatty Acid Metabolism
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