Evidence map›Paper›PMID 38385744›Full record

ArticleJCI insight2024

Aberrant miR-29 is a predictive feature of severe phenotypes in pediatric Crohn's disease.

Alexandria J Shumway, Michael T Shanahan, Emilie Hollville, Kevin Chen, Caroline Beasley, Jonathan W Villanueva, Sara Albert, Grace Lian, Moises R Cure, Matthew Schaner and 6 more

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
3.3field-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

4 citing papers in PubMed, 6 citations in OpenAlex.

  1. Review
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  3. Review
  4. 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

16 authors at 4 institutions in 2 countries.

Alexandria J ShumwayDepartment of Biomedical Sciences, Cornell University, Ithaca, New York, USA.
Michael T ShanahanDepartment of Biomedical Sciences, Cornell University, Ithaca, New York, USA.
Emilie HollvilleInstitute of Medical Sciences, University of Aberdeen Foresterhill, Aberdeen, Scotland, United Kingdom
Kevin ChenCenter for Gastrointestinal Biology and Disease.
Caroline BeasleyCenter for Gastrointestinal Biology and Disease.
Jonathan W VillanuevaDepartment of Biomedical Sciences, Cornell University, Ithaca, New York, USA.
Sara AlbertDepartment of Biomedical Sciences, Cornell University, Ithaca, New York, USA.
Grace LianCenter for Gastrointestinal Biology and Disease.
Moises R CureCenter for Gastrointestinal Biology and Disease.
Matthew SchanerCenter for Gastrointestinal Biology and Disease.
Lee-Ching ZhuDepartment of Pathology and Laboratory Medicine, and.
Surekha BantumilliDepartment of Pathology and Laboratory Medicine, and.
Mohanish DeshmukhNeuroscience Center.
Terrence S FureyCenter for Gastrointestinal Biology and Disease.
Shehzad Z SheikhCenter for Gastrointestinal Biology and Disease.
Praveen SethupathyDepartment of Biomedical Sciences, Cornell University, Ithaca, New York, USA.
Cornell University · USEmory University Hospital · USUniversity of Aberdeen · GBUniversity of North Carolina at Chapel Hill · US

Funding

Role of IL-10 in APC Regulation of Protective vs. Pathogenic T Cell Responses toP01DK094779 · NIDDK · UNIV OF NORTH CAROLINA CHAPEL HILL · PI SARTOR, RYAN B · 2013 to 2023
$17.9M
High throughput functional studies of IBD-associated GWAS variantsR01DK136262 · NIDDK · UNIV OF NORTH CAROLINA CHAPEL HILL · PI Terrence S. Furey, SHEHZAD Z. SHEIKH · 2023 to 2026
$2.6M
Discovery of aberrant enhancer activities during gut development that underlie genetic predisposition to pediatric Crohn's diseaseR21HD104922 · NICHD · CORNELL UNIVERSITY · PI SETHUPATHY, PRAVEEN · 2021 to 2022
$432k
NICHD NIH HHS R21 HD104922NIDDK NIH HHS P01 DK094779NIDDK NIH HHS R01 DK136262
6 · The paper itself

Abstract

Crohn's disease (CD) is a chronic inflammatory gut disorder. Molecular mechanisms underlying the clinical heterogeneity of CD remain poorly understood. MicroRNAs (miRNAs) are important regulators of gut physiology, and several have been implicated in the pathogenesis of adult CD. However, there is a dearth of large-scale miRNA studies for pediatric CD. We hypothesized that specific miRNAs uniquely mark pediatric CD. We performed small RNA-Seq of patient-matched colon and ileum biopsies from treatment-naive pediatric patients with CD (n = 169) and a control cohort (n = 108). Comprehensive miRNA analysis revealed 58 miRNAs altered in pediatric CD. Notably, multinomial logistic regression analysis revealed that index levels of ileal miR-29 are strongly predictive of severe inflammation and stricturing. Transcriptomic analyses of transgenic mice overexpressing miR-29 show a significant reduction of the tight junction protein gene Pmp22 and classic Paneth cell markers. The dramatic loss of Paneth cells was confirmed by histologic assays. Moreover, we found that pediatric patients with CD with elevated miR-29 exhibit significantly lower Paneth cell counts, increased inflammation scores, and reduced levels of PMP22. These findings strongly indicate that miR-29 upregulation is a distinguishing feature of pediatric CD, highly predictive of severe phenotypes, and associated with inflammation and Paneth cell loss.

Indexed as

Crohn DiseaseMicroRNAsAdultAnimalsChildHumansInflammationMicePhenotypeMicroRNAsMIRN29 microRNA, mouseGastroenterologyGeneticsInflammatory bowel disease

Identifiers

PMID38385744
PMCPMC10967384
OpenAlexW4392014948

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Registered trials

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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.