Evidence map›Paper›PMID 27852147›Full record

ArticleJournal of neurotrauma2017

RNA Binding Protein Human Antigen R Is Translocated in Astrocytes following Spinal Cord Injury and Promotes the Inflammatory Response.

Thaddaeus Kwan, Candace L Floyd, Soojin Kim, Peter H King

Abstract read
In one paragraph

Article in Journal of neurotrauma, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.4field-weighted citation impact, top 17% 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

24 citing papers in PubMed, 33 citations in OpenAlex.

  1. Review
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  6. Inhibition of the RNA Regulator HuR Mitigates Spinal Cord Injury by Potently Suppressing Post-Injury Neuroinflammation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  7. Article
  8. Exploring the Research Focus of RNA-Binding Proteins in Trauma and Burns.Analytical cellular pathology (Amsterdam) · 2024
    Review
  9. Article
  10. Article
  11. Article
  12. Inhibition of the RNA Regulator HuR by SRI-42127 Attenuates Neuropathic Pain After Nerve Injury Through Suppression of Neuroinflammatory Responses.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2022
    Article
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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

4 authors at 2 institutions in 1 country.

Thaddaeus Kwan1 Department of Neurology, University of Alabama , Birmingham, Alabama.
Candace L Floyd2 Department of Physical Medicine and Rehabilitation, University of Alabama , Birmingham, Alabama.
Soojin Kim1 Department of Neurology, University of Alabama , Birmingham, Alabama.
Peter H King1 Department of Neurology, University of Alabama , Birmingham, Alabama.
Birmingham VA Medical Center · USUniversity of Alabama at Birmingham · US

Funding

HuR and RNA regulation as a Novel Therapeutic Target in Malignant GliomaI01BX001706 · VA · BIRMINGHAM VA MEDICAL CENTER · PI KING, PETER H · 2015 to 2018
–
BLRD VA I01 BX001706
6 · The paper itself

Abstract

Inflammation plays a prominent role in the events following traumatic injury to the central nervous system (CNS). The initial inflammatory response is driven by mediators such as tumor necrosis factor α and interleukin 1β, which are produced by activated astrocytes and microglia at the site of injury. These factors are regulated post-transcriptionally by RNA binding proteins (RBP) that interact with adenylate and uridylate-rich elements (ARE) in the 3'-untranslated region of the messenger RNA (mRNA). Human antigen R (HuR) is one of these RBPs and generally functions as a positive regulator of ARE-containing mRNAs. Here, we hypothesized that HuR plays an important role in the induction of cytokine and chemokines in astrocytes following traumatic injury. Using a mouse model of spinal cord injury, we found HuR to be extensively translocated to the cytoplasm in astrocytes at the level of injury, consistent with its activation. In an in vitro stretch injury model of CNS trauma, we observed a similar cytoplasmic shift of HuR in astrocytes and an attenuation of cytokine induction with HuR knockdown. RNA kinetics and luciferase assays suggested that the effect was more related to transcription than RNA destabilization. A small molecule inhibitor of HuR suppressed cytokine induction of injured astrocytes and reduced chemoattraction for neutrophils and microglia. In summary, HuR is activated in astrocytes in the early stages of CNS trauma and positively regulates the molecular response of key inflammatory mediators in astrocytes. Our findings suggest that HuR may be a therapeutic target in acute CNS trauma for blunting secondary tissue injury triggered by the inflammatory response.

Indexed as

AnimalsAstrocytesDisease Models, AnimalELAV-Like Protein 1HumansInflammationMaleMiceMice, Inbred C57BLSpinal Cord InjuriesElavl1 protein, mouseELAV-Like Protein 1glial cell response to injuryinflammationmolecular biological approachesspinal cord injury

Identifiers

PMID27852147
PMCPMC5359693
OpenAlexW2581036117

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.