Evidence map›Paper›PMID 31220450›Full record

ArticleThe American journal of pathology2019

miR-24 Is Elevated in Ulcerative Colitis Patients and Regulates Intestinal Epithelial Barrier Function.

Artin Soroosh, Carl R Rankin, Christos Polytarchou, Zulfiqar A Lokhandwala, Ami Patel, Lin Chang, Charalabos Pothoulakis, Dimitrios Iliopoulos, David M Padua

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.7field-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

28 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Ion transport and epithelial barrier dysfunction in experimental models of ulcerative colitis.American journal of physiology. Gastrointestinal and liver physiology · 2025
    Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. 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

9 authors at 2 institutions in 1 country.

Artin SorooshVatche and Tamar Manoukian Division of Digestive Diseases, Department of Medicine, University of California, Los Angeles, Los Angeles, California.
Carl R RankinVatche and Tamar Manoukian Division of Digestive Diseases, Department of Medicine, University of California, Los Angeles, Los Angeles, California.
Christos PolytarchouVatche and Tamar Manoukian Division of Digestive Diseases, Department of Medicine, University of California, Los Angeles, Los Angeles, California.
Zulfiqar A LokhandwalaVatche and Tamar Manoukian Division of Digestive Diseases, Department of Medicine, University of California, Los Angeles, Los Angeles, California.
Ami PatelVatche and Tamar Manoukian Division of Digestive Diseases, Department of Medicine, University of California, Los Angeles, Los Angeles, California.
Lin ChangVatche and Tamar Manoukian Division of Digestive Diseases, Department of Medicine, University of California, Los Angeles, Los Angeles, California.
Charalabos PothoulakisVatche and Tamar Manoukian Division of Digestive Diseases, Department of Medicine, University of California, Los Angeles, Los Angeles, California.
Dimitrios IliopoulosVatche and Tamar Manoukian Division of Digestive Diseases, Department of Medicine, University of California, Los Angeles, Los Angeles, California.
David M PaduaVatche and Tamar Manoukian Division of Digestive Diseases, Department of Medicine, University of California, Los Angeles, Los Angeles, California; Division of Gastroenterology, Hepatology, and Parenteral Nutrition, Veterans Affairs Greater Los Angeles Healthcare System, Los Angeles, California. Electronic address: dpadua@mednet.ucla.edu.
University of California, Los Angeles · USVA Greater Los Angeles Healthcare System · US

Funding

UCLA Clinical Translational Science InstituteUL1TR001881 · NCATS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ARLEEN F. BROWN, ARASH NAEIM · 2016 to 2026
$118.1M
Pilot and Feasibility ProgramP30DK041301 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ROZENGURT, JUAN ENRIQUE · 1990 to 2019
$18.0M
Mechanisms of Neurotensin in Intestinal InflammationR01DK060729 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI POTHOULAKIS, CHARALABOS · 2002 to 2017
$5.0M
Characterization and Targeting of MiR-24 Network in ColitisR01DK110003 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI POTHOULAKIS, CHARALABOS · 2016 to 2020
$1.7M
NCATS NIH HHS UL1 TR001881NIDDK NIH HHS P30 DK041301NIDDK NIH HHS R01 DK060729NIDDK NIH HHS R01 DK110003
6 · The paper itself

Abstract

Inflammatory bowel disease is characterized by high levels of inflammation and loss of barrier integrity in the colon. The intestinal barrier is a dynamic network of proteins that encircle intestinal epithelial cells. miRNAs regulate protein-coding genes. In this study, miR-24 was found to be elevated in colonic biopsies and blood samples from ulcerative colitis (UC) patients compared with healthy controls. In the colon of UC patients, miR-24 is localized to intestinal epithelial cells, which prompted an investigation of intestinal epithelial barrier function. Two intestinal epithelial cell lines were used to study the effect of miR-24 overexpression on barrier integrity. Overexpression of miR-24 in both cell lines led to diminished transepithelial electrical resistance and increased dextran flux, suggesting an effect on barrier integrity. Overexpression of miR-24 did not induce apoptosis or affect cell proliferation, suggesting that the effect of miR-24 on barrier function was due to an effect on cell-cell junctions. Although the tight junctions in cells overexpressing miR-24 appeared normal, miR-24 overexpression led to a decrease in the tight junction-associated protein cingulin. Loss of cingulin compromised barrier formation; cingulin levels negatively correlated with disease severity in UC patients. Together, these data suggest that miR-24 is a significant regulator of intestinal barrier that may be important in the pathogenesis of UC.

Indexed as

Cell Membrane PermeabilityApoptosisCell ProliferationColitis, UlcerativeEpithelial CellsHumansIntestinesMicroRNAsTight JunctionsMicroRNAsMIRN24 microRNA, human

Identifiers

PMID31220450
PMCPMC6723227
OpenAlexW2949403791

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.