Evidence map›Paper›PMID 26618242›Full record

ArticleRNA biology2016

Long non-coding RNA ANRIL regulates inflammatory responses as a novel component of NF-κB pathway.

Xiao Zhou, Xiaorui Han, Ann Wittfeldt, Jingzhi Sun, Chujun Liu, Xiaoxia Wang, Li-Ming Gan, Huiqing Cao, Zicai Liang

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

Article in RNA biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 146 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
146citing papers in PubMed, 3 pooled it
5.9field-weighted citation impact, top 3% 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

146 citing papers in PubMed, 3 syntheses or guidelines pooled it, 236 citations in OpenAlex.

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86 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

9 authors at 3 institutions in 2 countries.

Xiao Zhoua Laboratory of Nucleic Acid Technology, Institute of Molecular Medicine, Peking University , Beijing , 100871 , China.
Xiaorui Hana Laboratory of Nucleic Acid Technology, Institute of Molecular Medicine, Peking University , Beijing , 100871 , China.
Ann Wittfeldtb Department of Molecular and Clinical Medicine , Institute of Medicine, Sahlgrenska Academy at the University of Gothenburg , Sweden.
Jingzhi Sunc Department of Cardiolody , Affiliated Hospital of Jining Medical University , Jining , 272000 , China.
Chujun Liud Beijing Key Laboratory of Cardiometabolic Molecular Medicine, Institute of Molecular Medicine, Peking University , Beijing , 100871 , China.
Xiaoxia Wanga Laboratory of Nucleic Acid Technology, Institute of Molecular Medicine, Peking University , Beijing , 100871 , China.
Li-Ming Ganb Department of Molecular and Clinical Medicine , Institute of Medicine, Sahlgrenska Academy at the University of Gothenburg , Sweden.
Huiqing Caoa Laboratory of Nucleic Acid Technology, Institute of Molecular Medicine, Peking University , Beijing , 100871 , China.
Zicai Lianga Laboratory of Nucleic Acid Technology, Institute of Molecular Medicine, Peking University , Beijing , 100871 , China.
Peking University · CNUniversity of Gothenburg · SEAffiliated Hospital of Jining Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Antisense Noncoding RNA in the INK4 Locus (ANRIL) is the prime candidate gene at Chr9p21, the well-defined genetic risk locus associated with multiple human diseases including coronary artery disease (CAD), while little is known regarding its role in the pathological processes. Endothelial dysfunction triggers atherosclerotic processes that are causatively linked to CAD. To evaluate the function of ANRIL in human endothelial cells (ECs), we examined ANRIL expression under pathological stimuli and found ANRIL was markedly induced by pro-inflammatory factors. Loss-of-function and chromatin immunoprecipitation approaches revealed that NF-κB mediates TNF-α induced ANRIL expression. RNA sequencing revealed that ANRIL silencing dysregulated expression of inflammatory genes including IL6 and IL8 under TNF-α treatment. We explored the regulatory mechanism of ANRIL on IL6/8 and found that Yin Yang 1 (YY1), an ANRIL binding transcriptional factor revealed by RNA immunoprecipitation, was required for IL6/8 expression under TNF-α treatment. YY1 was enriched at promoter loci of IL6/8 and ANRIL silencing impaired the enrichment, indicating a cooperation between ANRIL and YY1 in the regulation of inflammatory genes. For the first time, we establish the connection between ANRIL and NF-κB pathway and show that ANRIL regulates inflammatory responses through binding with YY1. The newly identified TNF-α-NF-κB-ANRIL/YY1-IL6/8 pathway enhances understanding of the etiology of CAD and provides potential therapeutic target for treatment of CAD.

Indexed as

Cell LineEndothelial CellsHumansHuman Umbilical Vein Endothelial CellsInterleukin-6Interleukin-8NF-kappa BPromoter Regions, GeneticRNA, Long NoncodingSignal TransductionTumor Necrosis Factor-alphaYY1 Transcription FactorCDKN2B antisense RNA, humanCXCL8 protein, humanIL6 protein, humanInterleukin-6Interleukin-8NF-kappa BRNA, Long NoncodingTumor Necrosis Factor-alphaYY1 protein, humanYY1 Transcription FactorANRILcoronary artery diseaseinflammationlong non-coding RNANF-κBYY1

Identifiers

PMID26618242
PMCPMC4829310
OpenAlexW2233535956

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.