Evidence map›Paper›PMID 34268386›Full record

ArticleAnnals of translational medicine2021

LncRNA NEAT1 mediates intestinal inflammation by regulating TNFRSF1B.

Shiyu Pan, Rui Liu, Xing Wu, Kejia Ma, Weiwei Luo, Kai Nie, Chao Zhang, Xiangrui Meng, Ting Tong, Xuejie Chen and 2 more

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Annals of translational medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 9% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.

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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

12 authors at 2 institutions in 1 country.

Shiyu PanDepartment of Gastroenterology, The Third Xiangya Hospital, Central South University, Changsha, China.
Rui LiuDepartment of Gastroenterology, The Third Xiangya Hospital, Central South University, Changsha, China.
Xing WuDepartment of Gastroenterology, The Third Xiangya Hospital, Central South University, Changsha, China.
Kejia MaDepartment of Gastroenterology, The Third Xiangya Hospital, Central South University, Changsha, China.
Weiwei LuoDepartment of Gastroenterology, The Third Xiangya Hospital, Central South University, Changsha, China.
Kai NieDepartment of Gastroenterology, The Third Xiangya Hospital, Central South University, Changsha, China.
Chao ZhangDepartment of Gastroenterology, The Third Xiangya Hospital, Central South University, Changsha, China.
Xiangrui MengDepartment of Gastroenterology, The Third Xiangya Hospital, Central South University, Changsha, China.
Ting TongDepartment of Gastroenterology, The Third Xiangya Hospital, Central South University, Changsha, China.
Xuejie ChenDepartment of Gastroenterology, The Third Xiangya Hospital, Central South University, Changsha, China.
Xiaoyan WangDepartment of Gastroenterology, The Third Xiangya Hospital, Central South University, Changsha, China.
Minzi DengDepartment of Gastroenterology, The Third Xiangya Hospital, Central South University, Changsha, China.
Third Xiangya Hospital · CNCentral South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundInflammatory bowel disease (IBD) is a chronic nonspecific intestinal disease. Our previous work showed that long non-coding RNA (LncRNA) nuclear enriched abundant transcript 1 (NEAT1) plays an important role in IBD. In the current study, we aimed to explore the underlying mechanism by which NEAT1 participates in the development of the disease.

methodsReal-time quantitative polymerase chain reaction (RT-qPCR) and western blotting were used to detect the expression of NEAT1 and tumor necrosis factor superfamily member 1B (TNFRSF1B) in clinical specimens and dextran sulfate sodium (DSS) colitis mice. Inflammatory cell models were established by stimulating human normal intestinal epithelial cell line NCM460 and human colon cancer cell line HT-29 with tumor necrosis factor alpha (TNF-α). Expressions of inflammatory cytokines such as interleukin-8 (IL-8) and monocyte chemoattractant protein-1 (MCP-1) were detected by enzyme-linked immunosorbent assay (ELISA) or RT-qPCR, TNFRSF1B, NF-κB p65 and p-NF-κB p65 followed by the knockdown or overexpression of NEAT1 and TNFRSF1B were analyzed by western blotting, and the regulatory effects of NEAT1 on TNFRSF1B were detected by RNA pull-down experiments and RNA-decay assay. The translocation of NF-κB p65 to the nucleus was detected by immunofluorescence.

resultsIn patients' specimens and DSS colitis mouse models, NEAT1 and TNFRSF1B expression were up-regulated compared with the control group. TNF-α stimulation increased NEAT1 and TNFRSF1B expression and activated NF-κB signaling pathway by increasing the translocation of NF-κB p65 to the nucleus. In the presence of TNF-α stimulation, NEAT1 knockdown reduces the expression of TNFRSF1B and the translocation of NF-κB p65, thereby relieves cell inflammation. These effects can be reversed by the overexpression of TNFRSF1B.In addition, NEAT1 is involved in inflammatory response by up-regulating the mRNA levels of TNFRSF1B, and knocking down NEAT1 can alleviate inflammation by down-regulating TNFRSF1B. Moreover, NEAT1 co-precipitates TNFRSF1B mRNA in RNA-pulldown assay, and the presence of NEAT1 stabilizes the mRNA of TNFRSF1B.

conclusionsOur results showed that LncRNA NEAT1 promotes NF-κB p65 translocation and mediates intestinal inflammation by regulating TNFRSF1B.

Indexed as

NF-κBNuclear enriched abundant transcript 1 (NEAT1)tumor necrosis factor superfamily member 1B (TNFRSF1B)ulcerative colitis

Identifiers

PMID34268386
PMCPMC8246228
OpenAlexW3163812861

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.