Evidence map›Paper›PMID 19884655›Full record

ArticleThe Journal of clinical investigation2009

Deletion of Pten in the mouse enteric nervous system induces ganglioneuromatosis and mimics intestinal pseudoobstruction.

Isabel Puig, Delphine Champeval, Pascal De Santa Barbara, Francis Jaubert, Stanislas Lyonnet, Lionel Larue

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

29 citing papers in PubMed, 58 citations in OpenAlex.

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  10. Akt phosphorylation of neuronal nitric oxide synthase regulates gastrointestinal motility in mouse ileum.Proceedings of the National Academy of Sciences of the United States of America · 2019
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  16. Adult enteric nervous system in health is maintained by a dynamic balance between neuronal apoptosis and neurogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2017
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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

6 authors at 6 institutions in 1 country.

Isabel PuigInstitut Curie, Centre de Recherche, Developmental Genetics of Melanocytes, Orsay, France.
Delphine Champeval
Pascal De Santa Barbara
Francis Jaubert
Stanislas Lyonnet
Lionel Larue
Assistance Publique – Hôpitaux de Paris · FRCentre National de la Recherche Scientifique · FRInserm · FRInstitut Curie · FRInstitut Necker Enfants Malades · FRMécanismes Adaptatifs et Evolution · FR

Funding

VITAMIN A DEFICIENCY AND INTESTINAL MOTILITY DISORDERSR01DK087715 · NIDDK · WASHINGTON UNIVERSITY · PI HEUCKEROTH, ROBERT O · 2010 to 2013
$1.3M
6 · The paper itself

Abstract

Intestinal ganglioneuromatosis is a benign proliferation of nerve ganglion cells, nerve fibers, and supporting cells of the enteric nervous system (ENS) that can result in abnormally large enteric neuronal cells (ENCs) in the myenteric plexus and chronic intestinal pseudoobstruction (CIPO). As phosphatase and tensin homolog deleted on chromosome 10 (PTEN) is a phosphatase that is critical for controlling cell growth, proliferation, and death, we investigated the role of PTEN in the ENS by generating mice with an embryonic, ENC-selective deletion within the Pten locus. Mutant mice died 2 to 3 weeks after birth, with clinical signs of CIPO and hyperplasia and hypertrophy of ENCs resulting from increased activity of the PI3K/PTEN-AKT-S6K signaling pathway. Further analysis revealed that PTEN was only expressed in developing mouse embryonic ENCs from E15.5 and that the rate of ENC proliferation decreased once PTEN was expressed. Specific deletion of the Pten gene in ENCs therefore induced hyperplasia and hypertrophy in the later stages of embryogenesis. This phenotype was reversed by administration of a pharmacological inhibitor of AKT. In some human ganglioneuromatosis forms of CIPO, PTEN expression was found to be abnormally low and S6 phosphorylation increased. Our study thus reveals that loss of PTEN disrupts development of the ENS and identifies the PI3K/PTEN-AKT-S6K signaling pathway as a potential therapeutic target for ganglioneuromatosis forms of CIPO.

Indexed as

AnimalsBase SequenceChronic DiseaseDisease Models, AnimalDNA PrimersEnteric Nervous SystemFemaleGanglioneuromaHumansImmunohistochemistryIntestinal Pseudo-ObstructionMaleMiceMice, Inbred C57BLMice, KnockoutMice, Mutant StrainsDNA PrimersPTEN PhosphohydrolasePten protein, mouse

Identifiers

PMID19884655
PMCPMC2786803
OpenAlexW2000690214

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.