Abstract
Das Gupta et al. show that HDAC7 and other class IIa HDAC enzymes control macrophage metabolism. They initiate TLR-inducible glycolysis in these cells and interact with the glycolytic enzyme PKM2 to drive inflammatory responses in vitro and in vivo. Class IIa HDAC inhibitors may have potential for attenuating immunometabolism-linked inflammation.
| Original language | English |
|---|---|
| Pages (from-to) | 2712-2728.e8 |
| Journal | Cell Reports |
| Volume | 30 |
| Issue number | 8 |
| DOIs | |
| Publication status | Published - 25 Feb 2020 |
| Externally published | Yes |
Keywords
- glycolysis
- histone deacetylases
- immunometabolism
- inflammation
- lysine acetylation
- macrophage
- post-translational modification
- pyruvate kinase
- toll-like receptor
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Class IIa Histone Deacetylases Drive Toll-like Receptor-Inducible Glycolysis and Macrophage Inflammatory Responses via Pyruvate Kinase M2. / Das Gupta, Kaustav; Shakespear, Melanie R.; Curson, James E.B. et al.
In: Cell Reports, Vol. 30, No. 8, 25.02.2020, p. 2712-2728.e8.Research output: Contribution to journal › Article › Research › peer-review
TY - JOUR
T1 - Class IIa Histone Deacetylases Drive Toll-like Receptor-Inducible Glycolysis and Macrophage Inflammatory Responses via Pyruvate Kinase M2
AU - Das Gupta, Kaustav
AU - Shakespear, Melanie R.
AU - Curson, James E.B.
AU - Murthy, Ambika M.V.
AU - Iyer, Abishek
AU - Hodson, Mark P.
AU - Ramnath, Divya
AU - Tillu, Vikas A.
AU - von Pein, Jessica B.
AU - Reid, Robert C.
AU - Tunny, Kathryn
AU - Hohenhaus, Daniel M.
AU - Moradi, Shayli Varasteh
AU - Kelly, Gregory M.
AU - Kobayashi, Takumi
AU - Gunter, Jennifer H.
AU - Stevenson, Alexander J.
AU - Xu, Weijun
AU - Luo, Lin
AU - Jones, Alun
AU - Johnston, Wayne A.
AU - Blumenthal, Antje
AU - Alexandrov, Kirill
AU - Collins, Brett M.
AU - Stow, Jennifer L.
AU - Fairlie, David P.
AU - Sweet, Matthew J.
N1 - Funding Information: This work was supported by a project grant (APP1047921) and an ideas grant (APP1184885) from the National Health and Medical Research Council (NHMRC) of Australia and an Australian Research Council Discovery Project (DP170102321). M.R.S. was supported by a University of Queensland Postdoctoral Fellowship. M.J.S. (APP1107914) and B.M.C. (APP1136021) are supported by NHMRC Senior Research Fellowships. D.P.F. is supported by NHMRC Senior Principal Research Fellowships (APP1027369 and APP1117017). K.A. is supported by an Australian Research Council (ARC) linkage project (LP150100689), an NHMRC program grant (APP1037320), and a CSIRO Future Science platform in synthetic biology. A.I. is supported by a University of Queensland Postdoctoral Fellowship and a University of Queensland Early Career Grant. L.L. is supported by an ARC Discovery Early Career Researcher Award (DECRA; DE180100524). We acknowledge the support of the Institute for Molecular Bioscience Dynamic Imaging Facility for Cancer Biology at The University of Queensland, established with the support of the Australian Cancer Research Foundation; the IMB Mass Spectrometry Facility; the Transgenic Animal Facility of Queensland (a division of The University of Queensland Biological Resources Department); and the ARC Centre of Excellence in Advanced Molecular Imaging (CE140100011). Metabolomics Australia is part of the Bioplatforms Australia network, funded through the Australian Government's National Collaborative Research Infrastructure Strategy (NCRIS). We thank Prof. Eric Olson and Dr. Rhonda Bassel-Duby for providing HDAC7fl/fl mice (UT Southwestern Medical Center), the Australian Red Cross Blood Service for providing buffy coats used in these studies, and Prof. Alpha Yap (IMB, The University of Queensland) for critical review of the manuscript. Conceptualization, M.R.S. K.D.G. A.I. D.P.F. and M.J.S.; Methodology, M.R.S. K.D.G. and M.J.S.; Formal Analysis, W.X.; Investigation, K.D.G. M.R.S. J.E.B.C. A.I. D.R. A.M.V.M. M.P.H. V.A.T. J.B.v.P. K.T. T.K. J.H.G. D.M.H. G.M.K. A.J.S. S.V.M. W.A.J. L.L. and A.J.; Resources, R.C.R.; Writing ? Original Draft, K.D.G. M.R.S. and M.J.S.; Writing ? Review & Editing, M.R.S. K.D.G. A.I. D.R. M.P.H. L.L. D.P.F. and M.J.S.; Supervision, M.R.S. W.J. K.A. B.M.C. A.B. J.L.S. D.P.F. and M.J.S.; Funding Acquisition, D.P.F. and M.J.S. The authors declare no competing interests. Funding Information: This work was supported by a project grant ( APP1047921 ) and an ideas grant ( APP1184885 ) from the National Health and Medical Research Council (NHMRC) of Australia and an Australian Research Council Discovery Project ( DP170102321 ). M.R.S. was supported by a University of Queensland Postdoctoral Fellowship. M.J.S. ( APP1107914 ) and B.M.C. ( APP1136021 ) are supported by NHMRC Senior Research Fellowships. D.P.F. is supported by NHMRC Senior Principal Research Fellowships ( APP1027369 and APP1117017 ). K.A. is supported by an Australian Research Council (ARC) linkage project ( LP150100689 ), an NHMRC program grant ( APP1037320 ), and a CSIRO Future Science platform in synthetic biology. A.I. is supported by a University of Queensland Postdoctoral Fellowship and a University of Queensland Early Career Grant. L.L. is supported by an ARC Discovery Early Career Researcher Award (DECRA; DE180100524 ). We acknowledge the support of the Institute for Molecular Bioscience Dynamic Imaging Facility for Cancer Biology at The University of Queensland , established with the support of the Australian Cancer Research Foundation ; the IMB Mass Spectrometry Facility ; the Transgenic Animal Facility of Queensland (a division of The University of Queensland Biological Resources Department ); and the ARC Centre of Excellence in Advanced Molecular Imaging ( CE140100011 ). Metabolomics Australia is part of the Bioplatforms Australia network, funded through the Australian Government’s National Collaborative Research Infrastructure Strategy (NCRIS). We thank Prof. Eric Olson and Dr. Rhonda Bassel-Duby for providing HDAC7 fl/fl mice (UT Southwestern Medical Center), the Australian Red Cross Blood Service for providing buffy coats used in these studies, and Prof. Alpha Yap (IMB, The University of Queensland) for critical review of the manuscript. Publisher Copyright: © 2020 The Author(s)
PY - 2020/2/25
Y1 - 2020/2/25
N2 - Das Gupta et al. show that HDAC7 and other class IIa HDAC enzymes control macrophage metabolism. They initiate TLR-inducible glycolysis in these cells and interact with the glycolytic enzyme PKM2 to drive inflammatory responses in vitro and in vivo. Class IIa HDAC inhibitors may have potential for attenuating immunometabolism-linked inflammation.
AB - Das Gupta et al. show that HDAC7 and other class IIa HDAC enzymes control macrophage metabolism. They initiate TLR-inducible glycolysis in these cells and interact with the glycolytic enzyme PKM2 to drive inflammatory responses in vitro and in vivo. Class IIa HDAC inhibitors may have potential for attenuating immunometabolism-linked inflammation.
KW - glycolysis
KW - histone deacetylases
KW - immunometabolism
KW - inflammation
KW - lysine acetylation
KW - macrophage
KW - post-translational modification
KW - pyruvate kinase
KW - toll-like receptor
UR - http://www.scopus.com/inward/record.url?scp=85079889717&partnerID=8YFLogxK
U2 - 10.1016/j.celrep.2020.02.007
DO - 10.1016/j.celrep.2020.02.007
M3 - Article
C2 - 32101747
AN - SCOPUS:85079889717
VL - 30
SP - 2712-2728.e8
JO - Cell Reports
JF - Cell Reports
SN - 2211-1247
IS - 8
ER -