Evidence map›Paper›PMID 29317607›Full record

ArticleCell death & disease2018

miRNA-3473b contributes to neuroinflammation following cerebral ischemia.

Xiaoyu Wang, Shuangshuang Chen, Jingshu Ni, Jian Cheng, Jia Jia, Xuechu Zhen

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed, 1 pooled it
6.4field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

54 citing papers in PubMed, 1 synthesis or guideline pooled it, 107 citations in OpenAlex.

  1. Pooled it
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  11. Role of miRNAs in neurovascular injury and repair.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2024
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Xiaoyu WangJiangsu Key Laboratory of Neuropsychiatric Diseases Research and College of Pharmaceutical Sciences, Soochow University, Suzhou, Jiangsu, 215021, China.
Shuangshuang ChenJiangsu Key Laboratory of Neuropsychiatric Diseases Research and College of Pharmaceutical Sciences, Soochow University, Suzhou, Jiangsu, 215021, China.
Jingshu NiJiangsu Key Laboratory of Neuropsychiatric Diseases Research and College of Pharmaceutical Sciences, Soochow University, Suzhou, Jiangsu, 215021, China.
Jian ChengJiangsu Key Laboratory of Neuropsychiatric Diseases Research and Institute of Neuroscience, Soochow University, Suzhou, China.
Jia JiaJiangsu Key Laboratory of Neuropsychiatric Diseases Research and College of Pharmaceutical Sciences, Soochow University, Suzhou, Jiangsu, 215021, China. jiajia@suda.edu.cn.
Xuechu ZhenJiangsu Key Laboratory of Neuropsychiatric Diseases Research and College of Pharmaceutical Sciences, Soochow University, Suzhou, Jiangsu, 215021, China. zhenxuechu@suda.edu.cn.
Soochow University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

3' Untranslated RegionsAnimalsAntagomirsBrain IschemiaCell HypoxiaCells, CulturedDisease Models, AnimalGlucoseInfarction, Middle Cerebral ArteryInterleukin-6MaleMiceMicrogliaMicroRNAsNeuronsNitric Oxide Synthase Type II3' Untranslated RegionsAntagomirsGlucoseInterleukin-6MicroRNAsNitric Oxide Synthase Type IISocs3 protein, mouseSuppressor of Cytokine Signaling 3 ProteinTumor Necrosis Factor-alpha

Identifiers

PMID29317607
PMCPMC5849032
OpenAlexW2783391945

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.