Evidence map›Paper›PMID 35016013›Full record

ArticleDevelopmental cell2022

Adaptive differentiation promotes intestinal villus recovery.

Takahiro E Ohara, Marco Colonna, Thaddeus S Stappenbeck

Abstract read
In one paragraph

Article in Developmental cell, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
–field-weighted citation impact
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

38 citing papers in PubMed.

  1. Review
  2. Review
  3. Article
  4. Fasting primes small intestinal regeneration after damage via a microbiome-metabolite-chromatin axis.Proceedings of the National Academy of Sciences of the United States of America · 2026
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors.

Takahiro E OharaDepartment of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA.
Marco ColonnaDepartment of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA.
Thaddeus S StappenbeckDepartment of Inflammation and Immunity, Lerner Research Institute, Cleveland Clinic, Cleveland, OH 44195, USA. Electronic address: stappet@ccf.org.

Funding

Washington University Center for Cellular ImagingP30CA091842 · NCI · WASHINGTON UNIVERSITY · PI AIMEE S JAMES · 2001 to 2026
$128.0M
CIS-REGULATORY CIRCUITS FOR ILC FUNCTION AND PLASTICITYR01AI134035 · NIAID · WASHINGTON UNIVERSITY · PI MARCO COLONNA, Eugene M Oltz · 2018 to 2026
$4.8M
The Role of Group 3 Innate Lymphoid cells (ILC3) in TuberculosisR01AI134236 · NIAID · WASHINGTON UNIVERSITY · PI COLONNA, MARCO, KHADER, SHABAANA A. · 2017 to 2021
$4.4M
Effects of inflammaging on intestinal epithelial cells and aspirin chemoprevention.R01CA257523 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI CHAN, ANDREW T, STAPPENBECK, THADDEUS S · 2021 to 2025
$3.7M
The role of TGFbeta in development and function of salivary gland innate lymphoid cellsR01DE025884 · NIDCR · WASHINGTON UNIVERSITY · PI COLONNA, MARCO, WEISMAN, GARY ANDREW · 2017 to 2021
$3.5M
Tunable therapeutic modulation of the gut microbiome by engineered probioticsR01AT009741 · NCCIH · WASHINGTON UNIVERSITY · PI DANTAS, GAUTAM, MOON, TAE SEOK · 2018 to 2022
$3.5M
Systemic Neurotropic virus infection effects on GI DysmotilityR01DK122790 · NIDDK · CLEVELAND CLINIC LERNER COM-CWRU · PI DIAMOND, MICHAEL S, HANDLEY, SCOTT A. · 2020 to 2023
$2.7M
Plasticity of Innate Lymphoid Cells: Mechanisms and Biological ImpactR01DK124699 · NIDDK · WASHINGTON UNIVERSITY · PI COLONNA, MARCO · 2020 to 2023
$1.4M
Mechanisms of Intestinal Villous RepairF30DK120076 · NIDDK · WASHINGTON UNIVERSITY · PI OHARA, TAKAHIRO ERICK · 2018 to 2019
$57k
NCCIH NIH HHS R01 AT009741NCI NIH HHS P30 CA091842NCI NIH HHS R01 CA257523NIAID NIH HHS R01 AI134035NIAID NIH HHS R01 AI134236NIDCR NIH HHS R01 DE025884NIDDK NIH HHS F30 DK120076NIDDK NIH HHS R01 DK122790NIDDK NIH HHS R01 DK124699
6 · The paper itself

Abstract

Loss of differentiated cells to tissue damage is a hallmark of many diseases. In slow-turnover tissues, long-lived differentiated cells can re-enter the cell cycle or transdifferentiate to another cell type to promote repair. Here, we show that in a high-turnover tissue, severe damage to the differentiated compartment induces progenitors to transiently acquire a unique transcriptional and morphological postmitotic state. We highlight this in an acute villus injury model in the mouse intestine, where we identified a population of progenitor-derived cells that covered injured villi. These atrophy-induced villus epithelial cells (aVECs) were enriched for fetal markers but were differentiated and lineage committed. We further established a role for aVECs in maintaining barrier integrity through the activation of yes-associated protein (YAP). Notably, loss of YAP activity led to impaired villus regeneration. Thus, we define a key repair mechanism involving the activation of a fetal-like program during injury-induced differentiation, a process we term "adaptive differentiation."

Indexed as

Adaptation, BiologicalAdaptor Proteins, Signal TransducingAnimalsCell CycleCell Cycle ProteinsCell DedifferentiationCell DifferentiationCell ProliferationEpithelial CellsFemaleIntestinal MucosaMaleMiceMice, Inbred C57BLModels, AnimalPhosphoproteinsAdaptor Proteins, Signal TransducingCell Cycle ProteinsPhosphoproteinsYap1 protein, mouseYAP-Signaling Proteinsadaptive differentiationenteropathyHippoinjury-repairintestinepoly(I:C)regenerationsingle-cell RNA sequencingvillus atrophyYAP

Identifiers

PMID35016013
PMCPMC9092613

What OpenQuestion holds

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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.