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University of California, Davis
Nat. Commun., 29 August 2026 | https://doi.org/10.1038/s41467-026-76159-2
Injury-transduced oligodendrocytes modulate neuroinflammation and glial activation in diseased and non-diseased central nervous system
Yan Wang1,2,8, Meina Zhu1,2,8, Joohyun Park1,2,8, Hyun Kyu Kim1,2, Ge Xiong1, Xi Chen3,4, Bo Chen5, Shinghua Ding6, Wensheng Lin7 & Fuzheng Guo1,2
1Department of Neurology, School of Medicine, University of California, Davis, Sacramento, CA, USA.
2Institute for Pediatric Regenerative Medicine (IPRM), Shriners Hospitals’ for Children– Northern California, Sacramento, CA, USA.
3Institute of Neurology, Sichuan Provincial People’s Hospital, Chengdu, China.
4School of Medicine, University of Electronic Science and Technology of China, Chengdu, China.
5Department of Neuroscience, Cell Biology and Anatomy, University of Texas Medical Branch, Galveston, TX, USA.
6Department of Chemical and Biomedical Engineering, University of Missouri, Columbia, MO, USA.
7Department of Neuroscience, University of Minnesota, Minneapolis, MN, USA.
8These authors contributed equally: Yan Wang, Meina Zhu, Joohyun Park.
Corresponding authors
Correspondence to Yan Wang or Fuzheng Guo.
1Department of Neurology, School of Medicine, University of California, Davis, Sacramento, CA, USA.
2Institute for Pediatric Regenerative Medicine (IPRM), Shriners Hospitals’ for Children– Northern California, Sacramento, CA, USA.
3Institute of Neurology, Sichuan Provincial People’s Hospital, Chengdu, China.
4School of Medicine, University of Electronic Science and Technology of China, Chengdu, China.
5Department of Neuroscience, Cell Biology and Anatomy, University of Texas Medical Branch, Galveston, TX, USA.
6Department of Chemical and Biomedical Engineering, University of Missouri, Columbia, MO, USA.
7Department of Neuroscience, University of Minnesota, Minneapolis, MN, USA.
8These authors contributed equally: Yan Wang, Meina Zhu, Joohyun Park.
Corresponding authors
Correspondence to Yan Wang or Fuzheng Guo.
Abstract
Oligodendrocytes (OLs) are brain cells that make myelin, the insulating sheath that supports nerve signal transmission. Although oligodendrocyte dysfunction is common in the central nervous system (CNS), how these cells respond to injury remains incompletely understood. Here we show, using mouse models and mouse tissue analyses, that OLs respond to demyelinating diseases by increasing the expression and secretion of serine protease inhibitor clade A member 3N (SERPINA3N). This transition of homeostatic OLs to Serpina3n-expressing OLs (SerpinOLs) occurs not only in demyelinating disease, but also after stroke, endotoxin-induced injury, neurodegeneration, traumatic injury, and healthy aging. Mechanistically, direct injury to OLs, rather than inflammation alone, drives the transition. Phenotypically, SerpinOLs show inflammatory and immune-regulatory features and activation of signal transducer and activator of transcription 3 (STAT3), which is required for SERPINA3N induction. Functionally, SerpinOLs amplify neuroinflammation and glial activation toward pro-inflammatory and neurodegenerative states. Together, SerpinOLs represent a common population of injury-transduced OLs that contributes to CNS pathology beyond myelin production.
논문정보
- Research article
- 2026년 08월 (BRIC 등록일 2026-09-02)
- 국외 연구진
- 생명과학 > 신경생물학
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