Evidence map›Paper›PMID 29253460›Full record

ArticleThe American journal of pathology2018

MicroRNA-31-3p Is Involved in Substance P (SP)-Associated Inflammation in Human Colonic Epithelial Cells and Experimental Colitis.

Kai Fang, Ivy Ka Man Law, David Padua, Aristea Sideri, Vanessa Huang, Christopher G Kevil, Dimitrios Iliopoulos, Charalabos Pothoulakis

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

21 citing papers in PubMed, 31 citations in OpenAlex.

  1. Trial
  2. Review
  3. Extracellular vesicle-mediated mechanisms and therapeutic potential in acute lung injury.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Review
  4. Article
  5. Review
  6. The Role of microRNAs in Inflammatory Bowel Disease.International journal of molecular sciences · 2025
    Review
  7. Article
  8. Review
  9. Review
  10. Review
  11. Review
  12. Review
  13. CSE/HFrontiers in immunology · 2022
    Article
  14. Review
  15. Article
  16. Review
  17. Review
  18. Review
  19. Knockout of the Tachykinin Receptor 1 in the Mdr2The American journal of pathology · 2020
    Article
  20. Review
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

8 authors at 2 institutions in 1 country.

Kai FangInflammatory Bowel Disease Center, Vatche and Tamar Manoukian Division of Digestive Diseases, David Geffen School of Medicine at University of California at Los Angeles, Los Angeles, California.
Ivy Ka Man LawInflammatory Bowel Disease Center, Vatche and Tamar Manoukian Division of Digestive Diseases, David Geffen School of Medicine at University of California at Los Angeles, Los Angeles, California.
David PaduaInflammatory Bowel Disease Center, Vatche and Tamar Manoukian Division of Digestive Diseases, David Geffen School of Medicine at University of California at Los Angeles, Los Angeles, California.
Aristea SideriInflammatory Bowel Disease Center, Vatche and Tamar Manoukian Division of Digestive Diseases, David Geffen School of Medicine at University of California at Los Angeles, Los Angeles, California.
Vanessa HuangInflammatory Bowel Disease Center, Vatche and Tamar Manoukian Division of Digestive Diseases, David Geffen School of Medicine at University of California at Los Angeles, Los Angeles, California.
Christopher G KevilDepartment of Pathology, Louisiana State University Health Sciences Center, Shreveport, Louisiana.
Dimitrios IliopoulosCenter for Systems Biomedicine, Vatche and Tamar Manoukian Division of Digestive Diseases, David Geffen School of Medicine at University of California at Los Angeles, Los Angeles, California.
Charalabos PothoulakisInflammatory Bowel Disease Center, Vatche and Tamar Manoukian Division of Digestive Diseases, David Geffen School of Medicine at University of California at Los Angeles, Los Angeles, California. Electronic address: cpothoulakis@mednet.ucla.edu.
University of California, Los Angeles · USLouisiana State University Health Sciences Center Shreveport · US

Funding

Women's CancersP30CA016042 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Robert Damoiseaux · 1985 to 2026
$134.5M
Pilot and Feasibility ProgramP30DK041301 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ROZENGURT, JUAN ENRIQUE · 1990 to 2019
$18.0M
Women's Health and Functional Visceral Disorders CenterP50DK064539 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI MAYER, EMERAN A · 2002 to 2017
$17.5M
Mechanisms of Neurotensin in Intestinal InflammationR01DK060729 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI POTHOULAKIS, CHARALABOS · 2002 to 2017
$5.0M
SUBSTANCE P AND INTESTINAL INFLAMMATIONR01DK047343 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI POTHOULAKIS, CHARALABOS · 1994 to 2014
$4.2M
Characterization and Targeting of MiR-24 Network in ColitisR01DK110003 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI POTHOULAKIS, CHARALABOS · 2016 to 2020
$1.7M
NCI NIH HHS P30 CA016042NIDDK NIH HHS P30 DK041301NIDDK NIH HHS P50 DK064539NIDDK NIH HHS R01 DK047343NIDDK NIH HHS R01 DK060729NIDDK NIH HHS R01 DK110003
6 · The paper itself

Abstract

Substance P (SP) mediates colitis. SP signaling regulates the expression of several miRNAs, including miR-31-3p, in human colonocytes. However, the role of miR-31-3p in colitis and the underlying mechanisms has not been elucidated. We performed real-time PCR analysis of miR-31-3p expression in human colonic epithelial cells overexpressing neurokinin-1 receptor (NCM460 NK-1R) in response to SP stimulation and in NCM460 cells after IL-6, IL8, tumor necrosis factor (TNF)-α, and interferon-γ exposure. Functions of miR-31-3p were tested in NCM460-NK-1R cells and the trinitrobenzene sulfonic acid (TNBS) and dextran sodium sulfate (DSS) models of colitis. Targets of miRNA-31-3p were confirmed by Western blot analysis and luciferase reporter assay. Jun N-terminal kinase inhibition decreased SP-induced miR-31-3p expression. miR-31-3p expression was increased in both TNBS- and DSS-induced colitis and human colonic biopsies from ulcerative colitis, compared with controls. Intracolonic administration of a miR-31-3p chemical inhibitor exacerbated TNBS- and DSS-induced colitis and increased colonic TNF-α, CXCL10, and chemokine (C-C motif) ligand 2 (CCL2) mRNA expression. Conversely, overexpression of miR-31-3p ameliorated the severity of DSS-induced colitis. Bioinformatic, luciferase reporter assay, and Western blot analyses identified RhoA as a target of miR-31-3p in NCM460 cells. Constitutive activation of RhoA led to increased expression of CCL2, IL6, TNF-α, and CXCL10 in NCM460-NK-1R cells on SP stimulation. Our results reveal a novel SP-miR-31-3p-RhoA pathway that protects from colitis. The use of miR-31-3p mimics may be a promising approach for colitis treatment.

Indexed as

AnimalsCell LineColitisColonCrohn DiseaseDextran SulfateDisease Models, AnimalEpithelial CellsHumansInflammationMAP Kinase Signaling SystemMiceMicroRNAsSubstance PDextran SulfateMicroRNAsMIRN31 microRNA, humanSubstance P

Identifiers

PMID29253460
PMCPMC5840489
OpenAlexW2774931787

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.