Evidence map›Paper›PMID 31656541›Full record

ArticleExperimental and therapeutic medicine2019

Long non-coding RNA-HOTAIR promotes the progression of sepsis by acting as a sponge of miR-211 to induce IL-6R expression.

Jianan Chen, Xingsheng Gu, Li Zhou, Shuguang Wang, Limei Zhu, Yangneng Huang, Feng Cao

Open access · diamondAbstract read
In one paragraph

Article in Experimental and therapeutic medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.5field-weighted citation impact, top 20% 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

17 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. lncHUB2: aggregated and inferred knowledge about human and mouse lncRNAs.Database : the journal of biological databases and curation · 2023
    Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Long Noncoding RNA: Regulatory Mechanisms and Therapeutic Potential in Sepsis.Frontiers in cellular and infection microbiology · 2021
    Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. HOTAIR inhibits the proliferation of glioblastoma cells by targeting miR-219.Cancer biomarkers : section A of Disease markers · 2020
    Article
  17. 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 1 institution in 1 country.

Jianan ChenDepartment of Emergency Intensive Care Unit, Ningbo 6th Hospital, Ningbo, Zhejiang 315040, P.R. China.
Xingsheng GuDepartment of Emergency, Ningbo 6th Hospital, Ningbo, Zhejiang 315040, P.R. China.
Li ZhouDepartment of Emergency Intensive Care Unit, Ningbo 6th Hospital, Ningbo, Zhejiang 315040, P.R. China.
Shuguang WangDepartment of Emergency Intensive Care Unit, Ningbo 6th Hospital, Ningbo, Zhejiang 315040, P.R. China.
Limei ZhuDepartment of Trauma Orthopedics, Ningbo 6th Hospital, Ningbo, Zhejiang 315040, P.R. China.
Yangneng HuangDepartment of Emergency, Ningbo 6th Hospital, Ningbo, Zhejiang 315040, P.R. China.
Feng CaoDepartment of Emergency, Ningbo 6th Hospital, Ningbo, Zhejiang 315040, P.R. China.
Ningbo No.6 Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sepsis remains the primary cause of death in intensive care units and multiple long non-coding RNAs (lncRNAs) have been demonstrated to be dysregulated in samples of patients with sepsis. However, whether lncRNA-HOTAIR is involved in the etiology of sepsis remains unclear. The aim of the present study was to investigate the role of HOTAIR in sepsis and to reveal the associated mechanisms. A bioinformatics analysis and dual-luciferase reporter assay was performed to evaluate the interaction between HOTAIR and miR-211, as well as miR-211 and IL-6R. An animal model of sepsis was established in mice via cecal ligation and puncture. Interferon (IFN)-γ, interleukin (IL)-6, IL-17, tumor necrosis factor (TNF)-α, IL-1β, IL-6 receptor (R), microRNA (miR)-211 and HOTAIR expression was measured using reverse transcription-quantitative PCR. Cellular proliferation and apoptosis of monocytes were assessed using cell counting kit-8 assay and flow cytometry, respectively. miR-211 was revealed to be targeted by HOTAIR and IL-6R. The expression of IFN-γ, IL-6, IL-17, TNF-α, IL-1β, IL-6R and HOTAIR was significantly upregulated in the septic mice, whereas miR-211 expression was downregulated. The overexpression of hox transcript antisense RNA (HOTAIR) and knockdown of miR-211 were associated with an increased expression of IFN-γ, IL-6, IL-17, TNF-α, IL-1β and IL-6R in monocytes, while the overexpression of miR-211 exhibited the opposite effect. HOTAIR overexpression and miR-211 knockdown significantly inhibited cellular proliferation and promoted monocyte apoptosis, whereas the overexpression of miR-211 exhibited the opposite effects in monocytes. Therefore, HOTAIR may promote the progression of sepsis by indirectly regulating the expression of IL-6R via miR-211.

Indexed as

apoptosiscecal ligation and puncturehox transcript antisense RNAinterleukin-6RmicroRNA-211sepsis

Identifiers

PMID31656541
PMCPMC6812472
OpenAlexW2976164466

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Registered trials

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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.