Evidence map›Paper›PMID 32474254›Full record

ArticleMolecular immunology2020

HuR promotes miRNA-mediated upregulation of NFI-A protein expression in MDSCs during murine sepsis.

Isatou Bah, Tuqa Alkhateeb, Ajinkya Kumbhare, Dima Youssef, Zhi Q Yao, Gregory A Hawkin, Charles E McCall, Mohamed El Gazzar

Erratum issuedOpen access · greenAbstract read
In one paragraph

Article in Molecular immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.1field-weighted citation impact, top 59% 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

3 citing papers in PubMed, 5 citations in OpenAlex.

  1. NamiRNA-Enhancer Network: The Changing Era Challenge and Chance of miRNA.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Review
  2. Article
  3. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

Isatou BahDepartment of Internal Medicine, East Tennessee State University College of Medicine, Johnson City, TN, 37614, USA.
Tuqa AlkhateebDepartment of Internal Medicine, East Tennessee State University College of Medicine, Johnson City, TN, 37614, USA.
Ajinkya KumbhareDepartment of Internal Medicine, East Tennessee State University College of Medicine, Johnson City, TN, 37614, USA.
Dima YoussefDepartment of Internal Medicine, East Tennessee State University College of Medicine, Johnson City, TN, 37614, USA.
Zhi Q YaoDepartment of Internal Medicine, East Tennessee State University College of Medicine, Johnson City, TN, 37614, USA.
Gregory A HawkinDepartment of Biochemistry and Center for Precision Medicine, Wake Forest University School of Medicine, Winston-Salem, NC, 27157, USA.
Charles E McCallDepartment of Internal Medicine, Wake Forest University School of Medicine, Winston-Salem, NC, 27157, USA.
Mohamed El GazzarDepartment of Internal Medicine, East Tennessee State University College of Medicine, Johnson City, TN, 37614, USA. Electronic address: elgazzar@etsu.edu.
East Tennessee State University · USWake Forest University · US

Funding

MicroRNAs and myeloid cell development during sepsisR01GM103887 · NIGMS · EAST TENNESSEE STATE UNIVERSITY · PI ELGAZZAR, MOHAMED A. · 2013 to 2018
$1.4M
NIGMS NIH HHS R01 GM103887
6 · The paper itself

Abstract

Myeloid-derived suppressor cells (MDSCs) contribute to high mortality rates during sepsis, but how sepsis induces MDSCs is unclear. Previously we reported that microRNA (miR)-21 and miR-181b reprogram MDSCs in septic mice by increasing levels of DNA binding transcription factor, nuclear factor 1 (NFI-A). Here, we provide evidence that miR-21 and miR-181b stabilize NFI-A mRNA and increase NFI-A protein levels by recruiting RNA-binding proteins HuR and Ago1 to its 3' untranslated region (3'UTR). We also find that the NFI-A GU-rich element (GRE)-binding protein CUGBP1 counters miR-21 and miR-181b dependent NFI-A mRNA stabilization and decreases protein production by replacing 3'UTR bound Ago1 with Ago2. We confirmed the miR-21 and miR-181b dependent reprogramming pathway in MDSCs transfected with a luciferase reporter construct containing an NFI-A 3'UTR fragment with point mutations in the miRNA binding sites. These results suggest that targeting NFI-A in MDSCs during sepsis may enhance resistance to uncontrolled infection.

Indexed as

AnimalsCells, CulturedELAV-Like Protein 1MaleMiceMice, Inbred BALB CMicroRNAsMyeloid-Derived Suppressor CellsNFI Transcription FactorsSepsisTranscriptional ActivationUp-RegulationElavl1 protein, mouseELAV-Like Protein 1MicroRNAsMIRN21 microRNA, mouseNfia protein, mouseNFI Transcription FactorsMDSCmiRNANFI-ASepsis

Identifiers

PMID32474254
PMCPMC7519576
OpenAlexW3028725318

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.