Evidence map›Paper›PMID 32017713›Full record

ArticleJCI insight2020

Dlx1/2 mice have abnormal enteric nervous system function.

Christina M Wright, James P Garifallou, Sabine Schneider, Heather L Mentch, Deepika R Kothakapa, Beth A Maguire, Robert O Heuckeroth

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

8 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. DLX genes and proteins in mammalian forebrain development.Development (Cambridge, England) · 2024
    Review
  6. Article
  7. scRNA-Seq Reveals New Enteric Nervous System Roles for GDNF, NRTN, and TBX3.Cellular and molecular gastroenterology and hepatology · 2021
    Article
  8. 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

7 authors at 1 institution in 2 countries.

Christina M WrightDepartment of Pediatrics.
James P GarifallouCenter for Applied Genomics, and.
Sabine SchneiderDepartment of Pediatrics.
Heather L MentchDepartment of Pediatrics.
Deepika R KothakapaDepartment of Pediatrics.
Beth A MaguireDepartment of Pediatrics.
Robert O HeuckerothDepartment of Pediatrics.
Children's Hospital of Philadelphia · US

Funding

VITAMIN A DEFICIENCY AND INTESTINAL MOTILITY DISORDERSR01DK087715 · NIDDK · WASHINGTON UNIVERSITY · PI HEUCKEROTH, ROBERT O · 2010 to 2013
$1.3M
Characterization of the Role of Dlx1 and Dlx2 in the Enteric Nervous SystemF30DK117546 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI WRIGHT, CHRISTINA MARIE · 2018 to 2019
$64k
NIDDK NIH HHS F30 DK117546NIDDK NIH HHS R01 DK087715
6 · The paper itself

Abstract

Decades ago, investigators reported that mice lacking DLX1 and DLX2, transcription factors expressed in the enteric nervous system (ENS), die with possible bowel motility problems. These problems were never fully elucidated. We found that mice lacking DLX1 and DLX2 (Dlx1/2-/- mice) had slower small bowel transit and reduced or absent neurally mediated contraction complexes. In contrast, small bowel motility seemed normal in adult mice lacking DLX1 (Dlx1-/-). Even with detailed anatomic studies, we found no defects in ENS precursor migration, or neuronal and glial density in Dlx1/2-/- or Dlx1-/- mice. However, RNA sequencing of Dlx1/2-/- ENS revealed dysregulation of many genes, including vasoactive intestinal peptide (Vip). Using immunohistochemistry and reporter mice, we then found that Dlx1/2-/- mice have reduced VIP expression and fewer VIP-lineage neurons in their ENS. Our study reveals what we believe is a novel connection between Dlx genes and Vip and highlights the observation that dangerous bowel motility problems can occur in the absence of easily identifiable ENS structural defects. These findings may be relevant for disorders like chronic intestinal pseudo-obstruction (CIPO) syndrome.

Indexed as

AnimalsEnteric Nervous SystemGastrointestinal MotilityGenes, LethalHomeodomain ProteinsMiceMice, Inbred C57BLMice, KnockoutTranscription FactorsDistal-less homeobox proteinsHomeodomain ProteinsTranscription FactorsDevelopmentEmbryonic developmentNeurodevelopmentNeuroscienceTranscription

Identifiers

PMID32017713
PMCPMC7101142
OpenAlexW3005270772

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.