Evidence map›Paper›PMID 28300326›Full record

ArticleGlia2017

HuR promotes the molecular signature and phenotype of activated microglia: Implications for amyotrophic lateral sclerosis and other neurodegenerative diseases.

Prachi Matsye, Lei Zheng, Ying Si, Soojin Kim, Wenyi Luo, David K Crossman, Preston E Bratcher, Peter H King

Open access · greenAbstract read
In one paragraph

Article in Glia, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

31 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
  2. Review
  3. Myeloid-specific tristetraprolin mitigates postsurgical incisional pain by suppressing proinflammatory responses.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. 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
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. 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
  15. Review
  16. Review
  17. Review
  18. Article
  19. Article
  20. Review
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

8 authors at 3 institutions in 1 country.

Prachi MatsyeDepartment of Neurology, University of Alabama, Birmingham, Alabama.
Lei ZhengDepartment of Neurology, University of Alabama, Birmingham, Alabama.
Ying SiDepartment of Neurology, University of Alabama, Birmingham, Alabama.
Soojin KimDepartment of Neurology, University of Alabama, Birmingham, Alabama.
Wenyi LuoDepartment of Pathology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma.
David K CrossmanDepartment of Genetics, University of Alabama, Birmingham, Alabama.
Preston E BratcherDepartment of Pediatrics, Division of Pediatric Pulmonary Medicine, National Jewish Health, Denver, Colorado.
Peter H KingDepartment of Neurology, University of Alabama, Birmingham, Alabama.ORCID 0000-0001-9391-7464
University of Alabama at Birmingham · USNational Jewish Health · USUniversity of Oklahoma Health Sciences Center · US

Funding

XRAY CRYSTALLOGRAPHYP30CA013148 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI Robert S Welner · 1985 to 2026
$165.9M
Virology CoreP30AI027767 · NIAID · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI OLAF KUTSCH · 1988 to 2026
$84.1M
Smad Signaling in Skeletal Muscle as a Biomarker of Disease Progression in ALSR01NS092651 · NINDS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI KING, PETER H · 2016 to 2020
$1.6M
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 BX001148BLRD VA I01 BX001706NCI NIH HHS P30 CA013148NIAID NIH HHS P30 AI027767NINDS NIH HHS R01 NS092651
6 · The paper itself

Abstract

In neurodegenerative diseases such as amyotrophic lateral sclerosis (ALS), chronic activation of microglia contributes to disease progression. Activated microglia produce cytokines, chemokines, and other factors that normally serve to clear infection or damaged tissue either directly or through the recruitment of other immune cells. The molecular program driving this phenotype is classically linked to the transcription factor NF-κB and characterized by the upregulation of proinflammatory factors such as IL-1β, TNF-α, and IL-6. Here, we investigated the role of HuR, an RNA-binding protein that regulates gene expression through posttranscriptional pathways, on the molecular and cellular phenotypes of activated microglia. We performed RNA sequencing of HuR-silenced microglia and found significant attenuation of lipopolysaccharide-induced IL-1β and TNF-α inflammatory pathways and other factors that promote microglial migration and invasion. RNA kinetics and luciferase reporter studies suggested that the attenuation was related to altered promoter activity rather than a change in RNA stability. HuR-silenced microglia showed reduced migration, invasion, and chemotactic properties but maintained viability. MMP-12, a target exquisitely sensitive to HuR knockdown, participates in the migration/invasion phenotype. HuR is abundantly detected in the cytoplasmic compartment of activated microglia from ALS spinal cords consistent with its increased activity. Microglia from ALS-associated mutant SOD1 mice demonstrated higher migration/invasion properties which can be blocked with HuR inhibition. These findings underscore an important role for HuR in sculpting the molecular signature and phenotype of activated microglia, and as a possible therapeutic target in ALS and other neurodegenerative diseases.

Indexed as

AdultAgedAmyotrophic Lateral SclerosisAnimalsBone Marrow CellsBrainCell LineCells, CulturedDisease Models, AnimalELAV-Like Protein 1FemaleGene Knockdown TechniquesHumansMaleMatrix Metalloproteinase 12Mice, Inbred C57BLELAVL1 protein, humanElavl1 protein, mouseELAV-Like Protein 1matrix metallopeptidase 12, mouseMatrix Metalloproteinase 12RNA, Messengercalyx of HeldEAATSlc38a3system Asystem N

Identifiers

PMID28300326
PMCPMC7944581
OpenAlexW2596059636

What OpenQuestion holds

Textmetadata
LicenceTDM
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.