Abstract |
Traumatic brain injury usually triggers glial scar formation, neuroinflammation, and neurodegeneration. However, the molecular mechanisms underlying these pathological features are largely unknown. Using a mouse model of hippocampal stab injury (HSI), we observed that miR-331, a brain-enriched microRNA, was significantly downregulated in the early stage (0-7 days) of HSI. Intranasal administration of agomir-331, an upgraded product of miR-331 mimics, suppressed reactive gliosis and neuronal apoptosis and improved cognitive function in HSI mice. Finally, we identified IL-1β as a direct downstream target of miR-331, and agomir-331 treatment significantly reduced IL-1β levels in the hippocampus after acute injury. Our findings highlight, for the first time, agomir-331 as a pivotal neuroprotective agent for early rehabilitation of HSI.
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Authors | Jin-Xing Wang, Xiao Xiao, Xuan-Cheng He, Bao-Dong He, Chang-Mei Liu, Zhao-Qian Teng |
Journal | Cells
(Cells)
Vol. 12
Issue 20
(10 11 2023)
ISSN: 2073-4409 [Electronic] Switzerland |
PMID | 37887272
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
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Topics |
- Humans
- Gliosis
- Neuroinflammatory Diseases
- Inflammation
(pathology)
- Brain Injuries, Traumatic
(complications, pathology)
- MicroRNAs
(genetics)
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