Targeting foam cell formation in inflammatory brain diseases by the histone modifier MS-275.


Journal

Annals of clinical and translational neurology
ISSN: 2328-9503
Titre abrégé: Ann Clin Transl Neurol
Pays: United States
ID NLM: 101623278

Informations de publication

Date de publication:
11 2020
Historique:
received: 08 07 2020
revised: 25 08 2020
accepted: 30 08 2020
pubmed: 1 10 2020
medline: 25 9 2021
entrez: 30 9 2020
Statut: ppublish

Résumé

To assess class I-histone deacetylase (HDAC) inhibition on formation of lipid-accumulating, disease-promoting phagocytes upon myelin load in vitro, relevant for neuroinflammatory disorders like multiple sclerosis (MS) and cerebral X-linked adrenoleukodystrophy (X-ALD). Immunohistochemistry on postmortem brain tissue of acute MS (n = 6) and cerebral ALD (n = 4) cases to analyze activation and foam cell state of phagocytes. RNA-Seq of in vitro differentiated healthy macrophages (n = 8) after sustained myelin-loading to assess the metabolic shift associated with foam cell formation. RNA-Seq analysis of genes linked to lipid degradation and export in MS-275-treated human HAP1 cells and RT-qPCR analysis of HAP1 cells knocked out for individual members of class I HDACs or the corresponding enzymatically inactive knock-in mutants. Investigation of intracellular lipid/myelin content after MS-275 treatment of myelin-laden human foam cells. Analysis of disease characteristic very long-chain fatty acid (VLCFA) metabolism and inflammatory state in MS-275-treated X-ALD macrophages. Enlarged foam cells coincided with a pro-inflammatory, lesion-promoting phenotype in postmortem tissue of MS and cerebral ALD patients. Healthy in vitro myelin laden foam cells upregulated genes linked to LXRα/PPARγ pathways and mimicked a program associated with tissue repair. Treating these cells with MS-275, amplified this gene transcription program and significantly reduced lipid and cholesterol accumulation and, thus, foam cell formation. In macrophages derived from X-ALD patients, MS-275 improved the disease-associated alterations of VLCFA metabolism and reduced the pro-inflammatory status of these cells. These findings identify class I-HDAC inhibition as a potential novel strategy to prevent disease promoting foam cell formation in CNS inflammation.

Identifiants

pubmed: 32997393
doi: 10.1002/acn3.51200
pmc: PMC7664285
doi:

Substances chimiques

Benzamides 0
Histone Deacetylase Inhibitors 0
Pyridines 0
entinostat 1ZNY4FKK9H

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

2161-2177

Subventions

Organisme : Austrian Science Fund FWF
ID : DOC 33
Pays : Austria
Organisme : Austrian Science Fund FWF
ID : P 28705
Pays : Austria

Informations de copyright

© 2020 The Authors. Annals of Clinical and Translational Neurology published by Wiley Periodicals LLC on behalf of American Neurological Association.

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Auteurs

Bettina Zierfuss (B)

Department of Pathobiology of the Nervous System, Centre for Brain Research, Medical University of Vienna, Vienna, 1090, Austria.

Isabelle Weinhofer (I)

Department of Pathobiology of the Nervous System, Centre for Brain Research, Medical University of Vienna, Vienna, 1090, Austria.

Agnieszka Buda (A)

Department of Pathobiology of the Nervous System, Centre for Brain Research, Medical University of Vienna, Vienna, 1090, Austria.

Niko Popitsch (N)

Institute of Molecular Biotechnology, Vienna, 1030, Austria.

Lena Hess (L)

Division of Cell and Developmental Biology, Center for Anatomy and Cell Biology, Medical University of Vienna, Vienna, 1090, Austria.

Verena Moos (V)

Division of Cell and Developmental Biology, Center for Anatomy and Cell Biology, Medical University of Vienna, Vienna, 1090, Austria.

Simon Hametner (S)

Department of Neuropathology and Neurochemistry, Medical University of Vienna, Vienna, 1090, Austria.

Stephan Kemp (S)

Laboratory Genetic Metabolic Diseases, Amsterdam UMC, Amsterdam Gastroenterology & Metabolism, Amsterdam Neuroscience, University of Amsterdam, Amsterdam, 1105AZ, The Netherlands.

Wolfgang Köhler (W)

Department of Neurology, University of Leipzig Medical Centre, Leukodystrophy Clinic, Leipzig, 04103, Germany.

Sonja Forss-Petter (S)

Department of Pathobiology of the Nervous System, Centre for Brain Research, Medical University of Vienna, Vienna, 1090, Austria.

Christian Seiser (C)

Division of Cell and Developmental Biology, Center for Anatomy and Cell Biology, Medical University of Vienna, Vienna, 1090, Austria.

Johannes Berger (J)

Department of Pathobiology of the Nervous System, Centre for Brain Research, Medical University of Vienna, Vienna, 1090, Austria.

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