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MAFB prevents excess inflammation after ischemic stroke by accelerating clearance of damage signals through MSR1
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MAFB prevents excess inflammation after ischemic stroke by accelerating clearance of damage signals through MSR1
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Journal Article
MAFB prevents excess inflammation after ischemic stroke by accelerating clearance of damage signals through MSR1
2017
Overview
The scavenger receptor MSR1 contributes to the clearance of damage-associated molecular patterns (DAMPs) by infiltrating myeloid cells in the post-stroke rodent brain. Myeloid cell MSR1 deficiency impairs clearance and exacerbates stroke-induced impairments, whereas a pharmacological intervention to boost MSR1 expression improves pathological and functional outcomes.
Damage-associated molecular patterns (DAMPs) trigger sterile inflammation after tissue injury, but the mechanisms underlying the resolution of inflammation remain unclear. In this study, we demonstrate that common DAMPs, such as high-mobility-group box 1 (HMGB1), peroxiredoxins (PRXs), and S100A8 and S100A9, were internalized through the class A scavenger receptors MSR1 and MARCO
in vitro
. In ischemic murine brain, DAMP internalization was largely mediated by MSR1. An elevation of MSR1 levels in infiltrating myeloid cells observed 3 d after experimental stroke was dependent on the transcription factor
Mafb
. Combined deficiency for
Msr1
and
Marco
, or for
Mafb
alone, in infiltrating myeloid cells caused impaired clearance of DAMPs, more severe inflammation, and exacerbated neuronal injury in a murine model of ischemic stroke. The retinoic acid receptor (RAR) agonist Am80 increased the expression of
Mafb
, thereby enhancing MSR1 expression. Am80 exhibited therapeutic efficacy when administered, even at 24 h after the onset of experimental stroke. Our findings uncover cellular mechanisms contributing to DAMP clearance in resolution of the sterile inflammation triggered by tissue injury.
Publisher
Nature Publishing Group US,Nature Publishing Group
Subject
/ 14/63
/ 38/61
/ 64/60
/ 82/51
/ Animals
/ Chromatin Immunoprecipitation
/ Infarction, Middle Cerebral Artery - immunology
/ Ischemia
/ MafB Transcription Factor - drug effects
/ MafB Transcription Factor - genetics
/ MafB Transcription Factor - immunology
/ Medicine
/ Mice
/ Proteins
/ R&D
/ Receptors, Immunologic - genetics
/ Receptors, Immunologic - immunology
/ Receptors, Retinoic Acid - agonists
/ Scavenger Receptors, Class A - drug effects
/ Scavenger Receptors, Class A - genetics
/ Scavenger Receptors, Class A - immunology
/ Science
/ Stroke
