Evidence map›Paper›PMID 31315126›Full record

ArticleJournal of innate immunity2020

Long Noncoding RNA Linc00632 Inhibits Interleukin-13-Induced Inflammatory Cytokine and Mucus Production in Nasal Epithelial Cells.

Liyan Yue, Xiaoyan Yin, Fang Hao, Jinhui Dong, Xiumin Ren, Ou Xu, Chunguang Shan

Open access · goldAbstract read
In one paragraph

Article in Journal of innate immunity, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 18% 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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.

  1. Pooled it
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  10. Review
  11. Article
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  13. Article
  14. [Research progress on the relationship between lncRNA and the pathogenesis of allergic rhinitis].Lin chuang er bi yan hou tou jing wai ke za zhi = Journal of clinical otorhinolaryngology head and neck surgery · 2022
    Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Noncoding RNAs and Virus and Treatment in Allergic Rhinitis.Evidence-based complementary and alternative medicine : eCAM · 2022
    Article
  20. Article
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

7 authors at 2 institutions in 1 country.

Liyan YueENT Department 1, The Second Hospital of Hebei Medical University, Shijiazhuang, China.
Xiaoyan YinENT Department 1, The Second Hospital of Hebei Medical University, Shijiazhuang, China.
Fang HaoENT Department 1, The Second Hospital of Hebei Medical University, Shijiazhuang, China.
Jinhui DongENT Department 1, The Second Hospital of Hebei Medical University, Shijiazhuang, China.
Xiumin RenENT Department 1, The Second Hospital of Hebei Medical University, Shijiazhuang, China.
Ou XuENT Department 1, The Second Hospital of Hebei Medical University, Shijiazhuang, China.
Chunguang ShanENT Department 1, The Second Hospital of Hebei Medical University, Shijiazhuang, China, scg19860421@163.com.
Second Hospital of Hebei Medical University · CNHebei Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Allergic rhinitis (AR) is an allergic disease characterized as (immunoglobulin E)-mediated type I hypersensitivity disorder. The interleukin-13 (IL-13) signaling pathway has been implicated in the pathogenesis of AR. In the present study, we investigated the regulatory role and mechanism of long noncoding RNA Linc00632 in IL-13-induced inflammatory cytokine and mucus production in nasal epithelial cells (NECs) from AR patients. We evaluated the expression of Linc00632 in nasal tissues from AR patients and in IL-13-treated NECs. We explored the role of Linc00632 in granulocyte-macrophage colony-stimulating factor (GM-CSF), eotaxin, and MUAC5AC production in IL-13-treated NECs. We searched for the potential target of Linc00632. Downregulation of Linc00632 was identified in nasal tissues of AR patients and in IL-13-treated NECs. Linc00632 inhibited IL-13-induced GM-CSF, eotaxin, and MUAC5AC production. Linc00632 targeted miR-498 and negatively regulated its expression. MiR-498 targeted IL1RN and inhibition of miR-498 suppressed IL-13-induced GM-CSF, eotaxin, and MUC5AC expression. The regulation of IL-13-induced dysfunction of NECs by Linc00632 depended on miR-498. Linc00632 inhibited IL-13-induced GM-CSF, eotaxin, and MUAC5AC production in IL-13-treated NECs by targeting miR-498.

Indexed as

Cells, CulturedChemokine CCL11Down-RegulationGranulocyte-Macrophage Colony-Stimulating FactorHumansHypersensitivity, ImmediateInflammation MediatorsInterleukin-13MicroRNAsMucusNasal MucosaRhinitis, AllergicRNA, Long NoncodingSignal TransductionChemokine CCL11Granulocyte-Macrophage Colony-Stimulating FactorInflammation MediatorsInterleukin-13MicroRNAsMIRN498 microRNA, humanRNA, Long NoncodingAllergic rhinitisGranulocyte-macrophage colony-stimulating factorInterleukin-13Linc00632Nasal epithelial cells

Identifiers

PMID31315126
PMCPMC6959101
OpenAlexW2956356077

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.