Evidence map›Paper›PMID 27492330›Full record

ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2016

A long noncoding RNA signature for ulcerative colitis identifies IFNG-AS1 as an enhancer of inflammation.

David Padua, Swapna Mahurkar-Joshi, Ivy Ka Man Law, Christos Polytarchou, John P Vu, Joseph R Pisegna, David Shih, Dimitrios Iliopoulos, Charalabos Pothoulakis

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

Article in American journal of physiology. Gastrointestinal and liver physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
84citing papers in PubMed, 1 pooled it
4.8field-weighted citation impact, top 4% 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

84 citing papers in PubMed, 1 synthesis or guideline pooled it, 120 citations in OpenAlex.

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24 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 2 institutions in 2 countries.

David PaduaDivision of Digestive Diseases, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, California;
Swapna Mahurkar-JoshiDivision of Digestive Diseases, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, California;
Ivy Ka Man LawDivision of Digestive Diseases, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, California;ORCID 0000-0002-7430-1215
Christos PolytarchouCenter for Systems Biomedicine, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, California; School of Science and Technology, Nottingham Trent University, Nottingham, United Kingdom;
John P VuDivision of Gastroenterology, Hepatology and Parenteral Nutrition, VA Greater Los Angeles Healthcare System and Department of Medicine David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, California; and.
Joseph R PisegnaDivision of Gastroenterology, Hepatology and Parenteral Nutrition, VA Greater Los Angeles Healthcare System and Department of Medicine David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, California; and.
David ShihInflammatory Bowel and Immunobiology Research Institute, Cedars-Sinai Medical Center, Los Angeles, California.
Dimitrios IliopoulosDivision of Digestive Diseases, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, California; Center for Systems Biomedicine, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, California;
Charalabos PothoulakisDivision of Digestive Diseases, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, California; cpothoulakis@mednet.ucla.edu.
University of California, Los Angeles · USCedars-Sinai Medical Center · US

Funding

Pilot and Feasibility ProgramP30DK041301 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ROZENGURT, JUAN ENRIQUE · 1990 to 2019
$18.0M
GASTROENTEROLOGYT32DK007180 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI JENSEN, DENNIS MICHAEL · 1986 to 2025
$10.0M
Mechanisms of Neurotensin in Intestinal InflammationR01DK060729 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI POTHOULAKIS, CHARALABOS · 2002 to 2017
$5.0M
NIDDK NIH HHS P30 DK041301NIDDK NIH HHS R01 DK060729NIDDK NIH HHS T32 DK007180
6 · The paper itself

Abstract

High-throughput technologies revealed new categories of genes, including the long noncoding RNAs (lncRNAs), involved in the pathogenesis of human disease; however, the role of lncRNAs in the ulcerative colitis (UC) has not been evaluated. Gene expression profiling was used to develop lncRNA signatures in UC samples. Jurkat T cells were activated by PMA/ionomycin subsequently interferon-γ (IFNG) and tumor necrosis factor (TNF)-α protein levels were assessed by ELISA. Anti-sense molecules were designed to block IFNG-AS1 expression. A unique set of lncRNAs was differentially expressed between UC and control samples. Of these, IFNG-AS1 was among the highest statistically significant lncRNAs (fold change: 5.27, P value: 7.07E-06). Bioinformatic analysis showed that IFNG-AS1 was associated with the IBD susceptibility loci SNP rs7134599 and its genomic location is adjacent to the inflammatory cytokine IFNG. In mouse models of colitis, active colitis samples had increased colonic expression of this lncRNA. Utilizing the Jurkat T cell model, we found IFNG-AS1 to positively regulate IFNG expression. Novel lncRNA signatures differentiate UC patients with active disease, patients in remission, and control subjects. A subset of these lncRNAs was found to be associated with the clinically validated IBD susceptibility loci. IFNG-AS1 was one of these differentially expressed lncRNAs in UC patients and found to regulate the key inflammatory cytokine, IFNG, in CD4 T cells. Taking these findings together, our study revealed novel lncRNA signatures deregulated in UC and identified IFNG-AS1 as a novel regulator of IFNG inflammatory responses, suggesting the potential importance of noncoding RNA mechanisms on regulation of inflammatory bowel disease-related inflammatory responses.

Indexed as

AdultAgedAnimalsCase-Control StudiesColitis, UlcerativeFemaleGene Expression RegulationHumansInflammationInterferon-gammaInterleukin-10Jurkat CellsMaleMiceMice, Inbred C57BLMice, KnockoutIFNG protein, humanIL10 protein, mouseInterferon-gammaInterleukin-10RNA, Long NoncodingRNA, Messengerinflammationinflammatory bowel diseaseinterferon γlncRNAulcerative colitis

Identifiers

PMID27492330
PMCPMC5076004
OpenAlexW2487363367

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.