Tregs depletion aggravates activation of astrocytes by modulating IL-10/GXP4 following cerebral infarction.
IL-10
astrocytes
cerebral infarction
ferroptosis
tregs
Journal
Frontiers in immunology
ISSN: 1664-3224
Titre abrégé: Front Immunol
Pays: Switzerland
ID NLM: 101560960
Informations de publication
Date de publication:
2023
2023
Historique:
received:
08
07
2023
accepted:
20
07
2023
medline:
28
8
2023
pubmed:
25
8
2023
entrez:
25
8
2023
Statut:
epublish
Résumé
Tregs plays a critical role in the development of secondary injuries in diseases. Accumulating evidence suggests an association between ischemic stroke and renal dysfunction; however, the underlying mechanisms remain unclear. This study aimed to investigate the potential of Tregs in inhibiting the activation of astrocytes after focal cerebral infarction. This study aimed to investigate the renal consequences of focal cerebral ischemia by subjecting a mouse model to transient middle cerebral artery occlusion (tMCAO). Subsequently, we assessed renal fibrosis, renal ferroptosis, Treg infiltration, astrocyte activation, as well as the expression levels of active GPX4, FSP1, IL-10, IL-6, and IL-2 after a 2-week period. In the tMCAO mouse model, depletion of tregs protected against activation of astrocyte and significantly decreased FSP1, IL-6, IL-2, and NLRP3 expression levels, while partially reversing the changes in Tregs. Mechanistically, tregs depletion attenuates renal fibrosis by modulating IL-10/GPX4 following cerebral infarction. Tregs depletion attenuates renal fibrosis by modulating IL-10/GPX4 following cerebral infarction.
Sections du résumé
Background
Tregs plays a critical role in the development of secondary injuries in diseases. Accumulating evidence suggests an association between ischemic stroke and renal dysfunction; however, the underlying mechanisms remain unclear. This study aimed to investigate the potential of Tregs in inhibiting the activation of astrocytes after focal cerebral infarction.
Methods
This study aimed to investigate the renal consequences of focal cerebral ischemia by subjecting a mouse model to transient middle cerebral artery occlusion (tMCAO). Subsequently, we assessed renal fibrosis, renal ferroptosis, Treg infiltration, astrocyte activation, as well as the expression levels of active GPX4, FSP1, IL-10, IL-6, and IL-2 after a 2-week period.
Results
In the tMCAO mouse model, depletion of tregs protected against activation of astrocyte and significantly decreased FSP1, IL-6, IL-2, and NLRP3 expression levels, while partially reversing the changes in Tregs. Mechanistically, tregs depletion attenuates renal fibrosis by modulating IL-10/GPX4 following cerebral infarction.
Conclusion
Tregs depletion attenuates renal fibrosis by modulating IL-10/GPX4 following cerebral infarction.
Identifiants
pubmed: 37622110
doi: 10.3389/fimmu.2023.1255316
pmc: PMC10446222
doi:
Substances chimiques
Interleukin-10
130068-27-8
Interleukin-2
0
Interleukin-6
0
glutathione peroxidase 4, mouse
EC 1.11.1.9
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1255316Informations de copyright
Copyright © 2023 Wang, Shi, Zhang, Yuan, Mao and Ma.
Déclaration de conflit d'intérêts
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. The reviewer DX declared a shared parent affiliation with the authors to the handling editor at the time of the review.
Références
Front Immunol. 2018 Oct 15;9:2356
pubmed: 30374354
Nat Commun. 2022 Apr 22;13(1):2206
pubmed: 35459868
Int Immunol. 2019 May 21;31(6):361-369
pubmed: 30893423
Neurosurg Focus. 2016 May;40(5):E2
pubmed: 27132523
Nat Rev Mol Cell Biol. 2021 Apr;22(4):266-282
pubmed: 33495651
Front Immunol. 2022 Jan 31;13:828447
pubmed: 35173738
Cell. 2018 Jul 12;174(2):285-299.e12
pubmed: 29887374
Nat Med. 2018 Jul;24(7):978-985
pubmed: 29942094
Cell Mol Biol Lett. 2020 Feb 27;25:10
pubmed: 32161620
Nature. 2019 Nov;575(7784):688-692
pubmed: 31634900
Cell Death Dis. 2020 Feb 3;11(2):88
pubmed: 32015325
Cell Death Discov. 2021 Jul 26;7(1):193
pubmed: 34312370
Theranostics. 2021 Jan 1;11(7):3052-3059
pubmed: 33537073
Nature. 2019 Nov;575(7784):693-698
pubmed: 31634899
Front Microbiol. 2023 Apr 05;14:1159986
pubmed: 37089576
Bioinformatics. 2018 Jul 1;34(13):i555-i564
pubmed: 29950010
Methods Mol Biol. 2019;1897:299-311
pubmed: 30539454
Front Chem. 2021 Oct 07;9:718405
pubmed: 34692637
Cell Death Differ. 2022 Nov;29(11):2190-2202
pubmed: 35534546
Nat Immunol. 2020 Jul;21(7):727-735
pubmed: 32541831
Kidney Int. 2021 Dec;100(6):1268-1281
pubmed: 34534552
Behav Anal Pract. 2022 Jan 3;15(2):505-514
pubmed: 35692516
Biomed Pharmacother. 2020 Jul;127:110108
pubmed: 32234642
Proc Natl Acad Sci U S A. 2022 Feb 15;119(7):
pubmed: 35140181
Nucleic Acids Res. 2017 Jan 4;45(D1):D353-D361
pubmed: 27899662
Exp Cell Res. 2021 Oct 15;407(2):112832
pubmed: 34536391
Annu Rev Med. 2021 Jan 27;72:281-311
pubmed: 33158368
Immunity. 2019 Feb 19;50(2):493-504.e7
pubmed: 30737144
Cell Death Dis. 2022 May 18;13(5):468
pubmed: 35585057
EBioMedicine. 2022 Feb;76:103847
pubmed: 35101656
Am J Respir Crit Care Med. 2021 Nov 1;204(9):1060-1074
pubmed: 34346860
Sci Immunol. 2018 Sep 14;3(27):
pubmed: 30217811
Nat Rev Immunol. 2022 Oct;22(10):614-628
pubmed: 35217787
Transl Stroke Res. 2017 Jul 17;:
pubmed: 28718030
Cell Death Differ. 2023 Feb;30(2):442-456
pubmed: 36443441
Signal Transduct Target Ther. 2022 Jun 20;7(1):196
pubmed: 35725836
Structure. 2016 Oct 4;24(10):1643-1657
pubmed: 27568928
Brain Circ. 2018 Jul-Sep;4(3):118-123
pubmed: 30450418
Nucleic Acids Res. 2019 Jan 8;47(D1):D330-D338
pubmed: 30395331
JCI Insight. 2022 Jan 11;7(1):
pubmed: 34793335
Cell. 2012 May 25;149(5):1060-72
pubmed: 22632970