Nrf2 controls homeostatic transcriptional signatures and inflammatory responses in a cell-type specific manner in the adult mouse brain

Summary: Nrf2 is a promising therapeutic target for neurological disorders, but its mechanisms of action remain unclear. While often linked to anti-inflammatory effects, this is mostly based on studies involving pharmacological activation. In the brain, Nrf2 is highly expressed in microglia, astrocy...

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Main Authors: Xin He, Owen Dando, Jing Qiu
Format: Article
Language:English
Published: Elsevier 2025-09-01
Series:iScience
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Online Access:http://www.sciencedirect.com/science/article/pii/S2589004225014592
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author Xin He
Owen Dando
Jing Qiu
author_facet Xin He
Owen Dando
Jing Qiu
author_sort Xin He
collection DOAJ
description Summary: Nrf2 is a promising therapeutic target for neurological disorders, but its mechanisms of action remain unclear. While often linked to anti-inflammatory effects, this is mostly based on studies involving pharmacological activation. In the brain, Nrf2 is highly expressed in microglia, astrocytes, and endothelial cells. As yet, the brain cell type-specific role of Nrf2 in regulating the basal transcriptome and controlling neuroinflammation is unknown. To address this, we employed three inducible conditional Nrf2 knockout mice in which Nrf2 is deleted in microglia, astrocytes, and brain endothelial cells, respectively. We discovered that in healthy brains, Nrf2 controls distinct transcriptional profiles in the three brain cell types under study. Surprisingly, after systemic inflammation, microglia, and astrocytes lacking Nrf2 showed reduced inflammatory responses, unlike endothelial cells. Additionally, even without any insult, Nrf2 in microglia supported the expression of pro-inflammatory genes. Our findings reveal a pro-inflammatory role for endogenous Nrf2 in specific brain cell types.
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institution Kabale University
issn 2589-0042
language English
publishDate 2025-09-01
publisher Elsevier
record_format Article
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spelling doaj-art-ff49f753ec2d464882b18fb2add2cf232025-08-20T04:00:55ZengElsevieriScience2589-00422025-09-0128911319810.1016/j.isci.2025.113198Nrf2 controls homeostatic transcriptional signatures and inflammatory responses in a cell-type specific manner in the adult mouse brainXin He0Owen Dando1Jing Qiu2UK Dementia Research Institute, University of Edinburgh, Edinburgh Medical School, 47 Little France Crescent, Edinburgh EH16 4TJ, UK; Centre for Discovery Brain Sciences, Edinburgh Medical School, University of Edinburgh, Edinburgh EH8 9XD, UK; Simons Initiative for the Developing Brain, Deanery of Biomedical Sciences, Edinburgh Medical School, University of Edinburgh, Edinburgh EH8 9XD, UKUK Dementia Research Institute, University of Edinburgh, Edinburgh Medical School, 47 Little France Crescent, Edinburgh EH16 4TJ, UK; Centre for Discovery Brain Sciences, Edinburgh Medical School, University of Edinburgh, Edinburgh EH8 9XD, UK; Simons Initiative for the Developing Brain, Deanery of Biomedical Sciences, Edinburgh Medical School, University of Edinburgh, Edinburgh EH8 9XD, UKUK Dementia Research Institute, University of Edinburgh, Edinburgh Medical School, 47 Little France Crescent, Edinburgh EH16 4TJ, UK; Centre for Discovery Brain Sciences, Edinburgh Medical School, University of Edinburgh, Edinburgh EH8 9XD, UK; Corresponding authorSummary: Nrf2 is a promising therapeutic target for neurological disorders, but its mechanisms of action remain unclear. While often linked to anti-inflammatory effects, this is mostly based on studies involving pharmacological activation. In the brain, Nrf2 is highly expressed in microglia, astrocytes, and endothelial cells. As yet, the brain cell type-specific role of Nrf2 in regulating the basal transcriptome and controlling neuroinflammation is unknown. To address this, we employed three inducible conditional Nrf2 knockout mice in which Nrf2 is deleted in microglia, astrocytes, and brain endothelial cells, respectively. We discovered that in healthy brains, Nrf2 controls distinct transcriptional profiles in the three brain cell types under study. Surprisingly, after systemic inflammation, microglia, and astrocytes lacking Nrf2 showed reduced inflammatory responses, unlike endothelial cells. Additionally, even without any insult, Nrf2 in microglia supported the expression of pro-inflammatory genes. Our findings reveal a pro-inflammatory role for endogenous Nrf2 in specific brain cell types.http://www.sciencedirect.com/science/article/pii/S2589004225014592biological sciencesneurosciencemolecular neuroscience
spellingShingle Xin He
Owen Dando
Jing Qiu
Nrf2 controls homeostatic transcriptional signatures and inflammatory responses in a cell-type specific manner in the adult mouse brain
iScience
biological sciences
neuroscience
molecular neuroscience
title Nrf2 controls homeostatic transcriptional signatures and inflammatory responses in a cell-type specific manner in the adult mouse brain
title_full Nrf2 controls homeostatic transcriptional signatures and inflammatory responses in a cell-type specific manner in the adult mouse brain
title_fullStr Nrf2 controls homeostatic transcriptional signatures and inflammatory responses in a cell-type specific manner in the adult mouse brain
title_full_unstemmed Nrf2 controls homeostatic transcriptional signatures and inflammatory responses in a cell-type specific manner in the adult mouse brain
title_short Nrf2 controls homeostatic transcriptional signatures and inflammatory responses in a cell-type specific manner in the adult mouse brain
title_sort nrf2 controls homeostatic transcriptional signatures and inflammatory responses in a cell type specific manner in the adult mouse brain
topic biological sciences
neuroscience
molecular neuroscience
url http://www.sciencedirect.com/science/article/pii/S2589004225014592
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AT owendando nrf2controlshomeostatictranscriptionalsignaturesandinflammatoryresponsesinacelltypespecificmannerintheadultmousebrain
AT jingqiu nrf2controlshomeostatictranscriptionalsignaturesandinflammatoryresponsesinacelltypespecificmannerintheadultmousebrain