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Cited by 53Neuroinflammation and Neurodegeneration MechanismsMicroRNA in disease regulationTraumatic Brain Injury and Neurovascular Disturbances

Knockdown of miR-155 protects microglia against LPS-induced inflammatory injury via targeting RACK1: a novel research for intracranial infection

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Yin, Haiyan, Song, Shuwen, Pan, Xudong·2017·Journal of Inflammation
DOI 10.1186/s12950-017-0162-7PMC PMC5549339
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Abstract

BACKGROUND: Intracranial infection, one of the complications of traumatic brain injury, is usually associated with inflammation. Several microRNAs (miRNAs), including miR-155, have been reported to be critical modulators in peripheral and central nervous system inflammation. In this study, we investigated the role of miR-155 in lipopolysaccharide (LPS)-induced inflammatory injury in mouse microglia BV2 cells. RESULTS: The expression level of miR-155 was significantly up-regulated after LPS stimulation in BV2 cells. LPS administration decreased BV2 cell viability, promoted apoptosis and increased the release of pro-inflammatory cytokines; while miR-155 knockdown rescued BV2 cell from LPS-induced injury. RACK1 was a directly target of miR-155. Interestingly, miR-155 knockdown did not attenuate LPS-induced inflammatory injury when RACK1 was knocked down. The mechanistic study indicated that miR-155 knockdown deactivated MAPK/NF-κB and mTOR signaling pathways under LPS-treated conditions. CONCLUSIONS: Knockdown of miR-155 protected mouse microglia BV2 cells from LPS-induced inflammatory injury via targeting RACK1 and deactivating MAPK/NF-κB and mTOR signaling pathways.

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  • Mice deficient in miR-155 have a diminished ability to respond to inflammatory stimuli, like LPS.

    “Mice deficient in miR-155 have a diminished ability to respond to inflammatory stimuli, like LPS [20, 21, 22]”

    From Microglia specific deletion of miR-155 in Alzheimer’s disease mouse models reduces amyloid-β pathology but causes hyperexcitability and seizures (2023) · cites this paper as [20]

    The Results section (no page provided) reports that miR-155 inhibition reduced inflammatory cytokine production in LPS-treated mouse microglial BV2 cells. This supports a diminished cellular response to LPS, but the study tested knockdown in cultured cells, not whether miR-155-deficient mice have a diminished response to inflammatory stimuli. (LLM, conf=0.88)

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Cited by

Sorted by citations

Authors
Yin, H., Song, S., & Pan, X.
Affiliations
  • Affiliated Hospital of Jining Medical University (CN)
  • Jining First People's Hospital (CN)
  • Affiliated Hospital of Qingdao University (CN)
Corresponding author
Pan, Xudong
ORCID
Pan, Xudong
Venue
Journal of Inflammation
Publisher
Springer Science and Business Media LLC
Published
2017-08-09
Volume
14
Issue
1
Pages
17-17
ISSN
1476-9255 (ISSN-L)
DOI
10.1186/s12950-017-0162-7
PMC
PMC5549339
OpenAlex
W2742882848
Cited by
53
References
3
Citations by year
2026: 2 · 2025: 3 · 2024: 9 · 2023: 6 · 2022: 6 · 2021: 7 · 2020: 7 · 2019: 6 · 2018: 7
FWCI
2.72
Type
journal article
Language
en
Update notices
correction (2018-04-03)
Open access
Licence
cc-by
Locations
  • Journal of Inflammation (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Topics
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
  • Health Sciences › Medicine › Neurology › Traumatic Brain Injury and Neurovascular Disturbances
Keywords
miR-155, RACK1, microglia, lipopolysaccharide, neuroinflammation, intracranial infection, traumatic brain injury, BV-2 cells, apoptosis, inflammatory cytokines, MAPK/NF-κB signaling, mTOR signaling, miRNA target genes

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