Cited by 110Neuroinflammation and Neurodegeneration MechanismsMicroRNA in disease regulationNeurological Disease Mechanisms and Treatments

miRNA-3473b contributes to neuroinflammation following cerebral ischemia.

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Wang, Xiaoyu, Chen, Shuangshuang, Ni, Jingshu, Cheng, Jian, Jia, Jia, Zhen, Xuechu·2018·Cell Death & Disease

Abstract

MicroRNAs play an essential role in stroke pathology. Here, we investigated the role of a newly identified microRNA, miR-3473b, in stroke pathology. The expression of miR-3473b was upregulated in the cortex and striatum in mice following transient middle cerebral artery occlusion (MCAO). Intracerebroventricular injection of the miR-3473b antagomir prior to MCAO remarkably attenuated ischemia-induced expression of miR-3473b and pro-inflammatory factors in the ischemic brain and decreased infarct volumes in mice following MCAO. Using in vitro approaches, we showed that the miR-3473b antagomir reduced the mRNA and protein levels of pro-inflammatory factors (iNOS, COX-2, TNF-α, and IL-6) in BV2 microglial cells subjected to LPS stimulation. The miR-3473b antagomir also decreased the expression of pro-inflammatory factors in BV2 cells activated with conditioned medium collected from oxygen-glucose deprivation (OGD)-treated neurons. Suppressor of cytokine signaling 3 (SOCS3), a physiological regulator of innate and adaptive immunity, was predicted to be a potential target of miR-3473b. We verified that the miR-3473b mimic decreased SOCS3 expression in BV2 cells. Meanwhile, the miR-3473b antagomir significantly increased both SOCS3 mRNA and protein levels in the BV2 cells treated with LPS as well as in the ischemic brain. By using the dual luciferase assay, we further showed that the 3'-untranslational region of SOCS3 was directly targeted by miR-3473b. In conclusion, induction of miR-3473b, which is likely targeted to SOCS3, contributes to stroke pathogenesis by enhancing post-stroke neuroinflammation injury.

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Authors
Wang, X., Chen, S., Ni, J., Cheng, J., Jia, J., & Zhen, X.
Affiliations
Soochow University (CN)
Corresponding author
  • Jia, Jia
  • Zhen, Xuechu
Venue
Cell Death & Disease
Published
2018-01-09
Volume
9
Issue
1
Pages
11-11
ISSN
2041-4889 (ISSN-L)
OpenAlex
W2783391945
Cited by
110
References
34
Citations by year
2026: 2 · 2025: 9 · 2024: 9 · 2023: 14 · 2022: 18 · 2021: 16 · 2020: 20 · 2019: 15 · 2018: 7
FWCI
6.52
Type
journal article
Language
en
Open access
Locations
  • Cell Death and Disease (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
Funders
  • National Natural Science Foundation of China (81671310, 81571124, BM2013003, 81373382, 81471336, 81371278, 81773702)
  • Priority Academic Program Development of Jiangsu Higher Education Institutions (BM2013003, 81571124, 81373382, 81371278)
Topics
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
  • Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
Keywords
microRNA, neuroinflammation, cerebral ischemia, stroke, SOCS3, microglia, BV-2 cells, middle cerebral artery occlusion, oxygen-glucose deprivation, inflammatory cytokines, inducible nitric oxide synthase, cyclooxygenase-2, TNF-α, interleukin-6, antagomir, 3' untranslated region
MeSH terms
Antagomirs, Suppressor of Cytokine Signaling 3 Protein, Animals, Cells, Cultured, Brain Ischemia, Disease Models, Animal, Glucose, Male, Neurons, Tumor Necrosis Factor-alpha, Cell Hypoxia, Interleukin-6, Microglia, Infarction, Middle Cerebral Artery, 3' Untranslated Regions, MicroRNAs, Mice, Nitric Oxide Synthase Type II

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