Induction of miR-155 after Brain Injury Promotes Type 1 Interferon and has a Neuroprotective Effect
Open accessAbstract
Traumatic brain injury produces profound and lasting neuroinflammation that has both beneficial and detrimental effects. Recent evidence has implicated microRNAs (miRNAs) in the regulation of inflammation both in the periphery and the CNS. We examined the expression of inflammation associated miRNAs in the context of traumatic brain injury using a mouse controlled cortical impact (CCI) model and found increased levels of miR-21, miR-223, and miR-155 in the hippocampus after CCI. The expression of miR-155 was elevated 9-fold after CCI, an increase confirmed by in situ hybridization. Interestingly, expression of miR-155 was largely found in neuronal nuclei as evidenced by co-localization with DAPI in MAP2 positive neurons. In miR-155 knock out mice expression of type I interferons IFNα and IFNβ, as well as interferon regulatory factor 1 and interferon-induced chemokine CXCL10 was decreased after TBI relative to WT mice. Unexpectedly, miR-155 KO mice had increased levels of microglial marker Iba1 and increased neuronal degeneration as measured by fluorojade C staining, suggesting a neuroprotective role for miR-155 in the context of TBI. This work demonstrates a role for miR-155 in regulation of the IFN response and neurodegeneration in the aftermath of TBI. While the presence of neuronal nuclear miRNAs has been described previously, their importance in disease states is relatively unknown. Here, we show evidence of dynamic regulation and pathological function of a nuclear miRNA in TBI.
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Since many disorders share the same proteins or micro RNAs as markers, it is impossible to have selective detection of diseases.
“Also, since many disorders share the same proteins or micro RNAs as markers, it is impossible to have selective detection of diseases [313–317].”
From Extracellular vesicles as nanotheranostic platforms for targeted neurological disorder interventions (2024) · cites this paper as [316]
The Discussion (page not available) describes miR-155 as having roles in several neurological disease models, supporting the narrower point that one microRNA is associated with multiple disorders. It does not establish that these microRNAs or proteins are shared diagnostic markers, or that selective disease detection is impossible. (LLM, conf=0.84)
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- Authors
- Harrison, E. B., Emanuel, K., Lamberty, B. G., Morsey, B. M., Li, M., Kelso, M. L., Yelamanchili, S. V., & Fox, H. S.
- Affiliations
- Nebraska Medical Center (US)
- Corresponding author
- Fox, Howard S.
- Venue
- Frontiers in Molecular Neuroscience
- Publisher
- Frontiers Media SA
- Published
- 2017-07-28
- Volume
- 10
- Pages
- 228-228
- ISSN
- 1662-5099 (ISSN-L)
- PMC
- PMC5532436
- OpenAlex
- W2734372389
- Cited by
- 48
- References
- 72
- Citations by year
- 2026: 3 · 2025: 4 · 2024: 3 · 2023: 1 · 2022: 4 · 2021: 5 · 2020: 10 · 2019: 5 · 2018: 11 · 2017: 2
- FWCI
- 5.33
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- Frontiers in Molecular Neuroscience (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Carolina Digital Repository (University of North Carolina at Chapel Hill) (submittedVersion)
- DigitalCommons@UNMC (submittedVersion, cc-by)
- Creighton Digital Repository (CDR) (submittedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- UNC Libraries
- Funders
- University of Nebraska Medical Center
- National Cancer Institute (T32CA196589)
- Topics
- Health Sciences › Medicine › Neurology › Traumatic Brain Injury and Neurovascular Disturbances
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- miR-155, traumatic brain injury, type I interferon, neuroinflammation, neuroprotection, controlled cortical impact, hippocampus, microglia, neurodegeneration, IRF1, CXCL10, miR-21, miR-223
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