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Cited by 112Neuroinflammation and Neurodegeneration MechanismsMicroRNA in disease regulationAcute Ischemic Stroke Management

In vivo inhibition of miR-155 significantly alters post-stroke inflammatory response

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Pena-Philippides, Juan Carlos, Caballero-Garrido, Ernesto, Lordkipanidze, Tamar, Roitbak, Tamara·2016·Journal of Neuroinflammation
DOI 10.1186/s12974-016-0753-xPMC PMC5103429
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Abstract

BACKGROUND: MicroRNA miR-155 is implicated in modulation of the inflammatory processes in various pathological conditions. In our previous studies, we demonstrated that in vivo inhibition of miR-155 promotes functional recovery after mouse experimental stroke. In the present study, we explored if this beneficial effect is associated with miR-155 inhibition-induced alterations in post-stroke inflammatory response. METHODS: Intravenous injections of a specific miR-155 inhibitor were initiated at 48 h after mouse distal middle cerebral artery occlusion (dMCAO). Temporal changes in the expression of cytokines and key molecules associated with cytokine signaling were assessed at 7, 14, and 21 days after dMCAO, using mouse cytokine gene and protein arrays and Western blot analyses. Electron and immunofluorescence confocal microscopy techniques were used to evaluate the ultrastructural changes, as well as altered expression of specific phenotypic markers, at different time points after dMCAO. RESULTS: In the inhibitor-injected mice (inhibitor group), there was a significant decrease in CCL12 and CXCL3 cytokine expression at 7 days and significantly increased levels of major cytokines IL-10, IL-4, IL-6, MIP-1α, IL-5, and IL-17 at 14 days after dMCAO. These temporal changes correlated with altered expression of miR-155 target proteins SOCS-1, SHIP-1, and C/EBP-β and phosphorylation levels of cytokine signaling regulator STAT-3. Electron microscopy showed decreased number of phagocytically active peri-vascular microglia/macrophages in the inhibitor samples. Immunofluorescence and Western blot of these samples demonstrated that expression of leukocyte/ macrophage marker CD45 and phagocytosis marker CD68 was reduced at 7 days, and in contrast, significantly increased at 14 days after dMCAO, as compared to controls. CONCLUSIONS: Based on our findings, we propose that in vivo miR-155 inhibition following mouse stroke significantly alters the time course of the expression of major cytokines and inflammation-associated molecules, which could influence inflammation process and tissue repair after experimental cerebral ischemia.

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  • In vivo inhibition of miR-155 in mice during stroke leads to derepression of SOCS-1, SHIP-1, and C/EBP-β and increased STAT-3 phosphorylation, resulting in upregulation of IL-10, IL-4, IL-6, MIP-1α, IL-5, and IL-17.

    “It was further demonstrated that in vivo inhibition of miR-155 in mice during an experiment on strokes leads to derepression of SOCS-1, SHIP-1 (interaction demonstrated in [158]) and C/EBP-β (interaction demonstrated in [245]) and increased phosphorylation levels of cytokine signaling regulator STAT-3. These changes result in upregulation of anti-inflammatory cytokines, namely IL-10, IL-4, IL-6, M”

    From MicroRNAs as Regulators of Phagocytosis (2022) · cites this paper as [246]

    The Results sections report increased SOCS-1, SHIP-1, and C/EBP-β at 7 days after stroke, and increased levels of all six listed cytokines at 14 days. But STAT-3 phosphorylation decreased at 7 days and increased only at 14 days, when SOCS-1 and SHIP-1 were no longer elevated. The paper describes possible links among these changes rather than establishing that they caused the cytokine increases; it also does not classify all six cytokines as anti-inflammatory. (LLM, conf=0.89)

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Cited by

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Authors
Pena-Philippides, J. C., Caballero-Garrido, E., Lordkipanidze, T., & Roitbak, T.
Affiliations
  • Ilia State University (GE)
  • University of New Mexico (US)
Corresponding author
Roitbak, Tamara
ORCID
Venue
Journal of Neuroinflammation
Publisher
Springer Science and Business Media LLC
Published
2016-11-09
Volume
13
Issue
1
Pages
287-287
ISSN
1742-2094 (ISSN-L)
DOI
10.1186/s12974-016-0753-x
PMC
PMC5103429
OpenAlex
W2552573152
Cited by
112
References
4
Citations by year
2026: 6 · 2025: 6 · 2024: 11 · 2023: 4 · 2022: 12 · 2021: 12 · 2020: 16 · 2019: 25 · 2018: 10 · 2017: 9 · 2015: 1
FWCI
8.04
Type
journal article
Language
en
Open access
Licence
Locations
  • Journal of Neuroinflammation (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
Funders
National Institute of Neurological Disorders and Stroke (R01NS082225)
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 › Epidemiology › Acute Ischemic Stroke Management
Keywords
miR-155, microRNA inhibition, post-stroke inflammation, cerebral ischemia, middle cerebral artery occlusion, cytokine expression, STAT3 signaling, SOCS1, SHIP1, C/EBPβ, microglia/macrophages, phagocytosis, CD68, CD45, neuroinflammation, tissue repair
MeSH terms
Antagomirs, Suppressor of Cytokine Signaling 1 Protein, Phosphatidylinositol-3,4,5-Trisphosphate 5-Phosphatases, Animals, Calcium-Binding Proteins, Disease Models, Animal, Encephalitis, Gene Expression Regulation, Macrophages, Male, Mice, Inbred C57BL, Microfilament Proteins, Time Factors, Signal Transduction, Cytokines, Microglia, Infarction, Middle Cerebral Artery, MicroRNAs, CREB-Binding Protein, Mice

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