Evidence map›Paper›PMID 24608041›Full record

ArticleNature immunology2014

Negative regulation of Hif1a expression and TH17 differentiation by the hypoxia-regulated microRNA miR-210.

Haopeng Wang, Henrik Flach, Michio Onizawa, Lai Wei, Michael T McManus, Arthur Weiss

Open access · greenAbstract read
In one paragraph

Article in Nature immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 148 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
148citing papers in PubMed, 1 pooled it
11.4field-weighted citation impact, top 1% 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

148 citing papers in PubMed, 1 synthesis or guideline pooled it, 251 citations in OpenAlex.

  1. Pooled it
  2. Plasma levels of microRNA in chronic kidney disease: patterns in acute and chronic exercise.American journal of physiology. Heart and circulatory physiology · 2015
    Trial
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  7. CAP-CD56Bioactive materials · 2026
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  9. Review
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  11. Review
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  14. Metabolic Stress Expands Polyfunctional, Proinflammatory ThArthritis & rheumatology (Hoboken, N.J.) · 2025
    Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Review

88 more citing papers are in PubMed but not listed here.

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 3 institutions in 2 countries.

Haopeng Wang *Departments of Medicine and of Microbiology & Immunology, the Rosalind Russell-Ephraim P. Engleman Medical Research Center for Arthritis, and the Howard Hughes Medical Institute, University of California, San Francisco, CA 94143.
Henrik Flach *Departments of Medicine and of Microbiology & Immunology, the Rosalind Russell-Ephraim P. Engleman Medical Research Center for Arthritis, and the Howard Hughes Medical Institute, University of California, San Francisco, CA 94143.
Michio OnizawaDepartment of Medicine University of California, San Francisco.
Lai WeiState Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangzhou, China.
Michael T McManusDiabetes Center, University of California, San Francisco.
Arthur WeissDepartments of Medicine and of Microbiology & Immunology, the Rosalind Russell-Ephraim P. Engleman Medical Research Center for Arthritis, and the Howard Hughes Medical Institute, University of California, San Francisco, CA 94143.
Howard Hughes Medical Institute · USUniversity of California, San Francisco · USSun Yat-sen University · CN

Funding

Howard Hughes Medical Institute
6 · The paper itself

Abstract

The microRNA miR-210 is a signature of hypoxia. We found robust increase in the abundance of miR-210 (>100-fold) in activated T cells, especially in the TH17 lineage of helper T cells. Hypoxia acted in synergy with stimulation via the T cell antigen receptor (TCR) and coreceptor CD28 to accelerate and increase Mir210 expression. Mir210 was directly regulated by HIF-1α, a key transcriptional regulator of TH17 polarization. Unexpectedly, we identified Hif1a as a target of miR-210, which suggested negative feedback by miR-210 in inhibiting HIF-1α expression. Deletion of Mir210 promoted TH17 differentiation under conditions of limited oxygen. In experimental colitis, miR-210 reduced the abundance of Hif1a transcripts and the proportion of cells that produced inflammatory cytokines and controlled disease severity. Our study identifies miR-210 as an important regulator of T cell differentiation in hypoxia, which can limit immunopathology.

Indexed as

AnimalsCD4 AntigensCell DifferentiationCell HypoxiaCells, CulturedColitis, UlcerativeCytokinesDisease Models, AnimalDisease ProgressionHumansHypoxia-Inducible Factor 1, alpha SubunitLymphocyte ActivationMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicCD4 AntigensCytokinesHif1a protein, mouseHypoxia-Inducible Factor 1, alpha SubunitMicroRNAsMIRN210 microRNA, mouse

Identifiers

PMID24608041
PMCPMC3996831
OpenAlexW2086513198

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.