Evidence map›Paper›PMID 22383494›Full record

ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2012

p38 MAPK regulates Bax activity and apoptosis in enterocytes at baseline and after intestinal resection.

Derek Wakeman, Jun Guo, Jethrina A Santos, Wambui S Wandu, John E Schneider, Mark E McMellen, Jennifer A Leinicke, Christopher R Erwin, Brad W Warner

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Gastrointestinal and liver physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

20 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Review
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  4. Article
  5. A novel maladaptive unfolded protein response as a mechanism for small bowel resection-induced liver injury.American journal of physiology. Gastrointestinal and liver physiology · 2022
    Article
  6. Article
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  8. Liver injury after small bowel resection is prevented in obesity-resistant 129S1/SvImJ mice.American journal of physiology. Gastrointestinal and liver physiology · 2021
    Article
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  16. Review
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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

9 authors at 1 institution in 1 country.

Derek WakemanDepartment of Surgery, Division of Pediatric Surgery, St. Louis Children's Hospital, Washington University School of Medicine, St. Louis, Missouri 63110, USA.
Jun Guo
Jethrina A Santos
Wambui S Wandu
John E Schneider
Mark E McMellen
Jennifer A Leinicke
Christopher R Erwin
Brad W Warner
St. Louis Children's Hospital · US

Funding

Large Scale Genome SequencingU54HG003079 · NHGRI · WASHINGTON UNIVERSITY · PI DUTCHER, SUSAN K · 2004 to 2016
$445.7M
Washington University DDRCC Supplemental Equipment RequestP30DK052574 · NIDDK · WASHINGTON UNIVERSITY · PI Nicholas O. Davidson · 2000 to 2026
$30.8M
SURGICAL ONCOLOGY TRAINING GRANTT32CA009621 · NCI · WASHINGTON UNIVERSITY · PI TIMOTHY J. EBERLEIN, William E. Gillanders · 1988 to 2026
$12.9M
ENTEROCYTE APOPTOSIS AFTER INTESTINAL RESECTIONR01DK059288 · NIDDK · WASHINGTON UNIVERSITY · PI WARNER, BRAD WAYNE · 2002 to 2011
$3.2M
NCI NIH HHS T32 CA009621NHGRI NIH HHS U54 HG003079NIDDK NIH HHS P30 DK052574NIDDK NIH HHS R01 DK 059288NIDDK NIH HHS R01 DK059288
6 · The paper itself

Abstract

Increased apoptosis in crypt enterocytes is a key feature of intestinal adaptation following massive small bowel resection (SBR). Expression of the proapoptotic factor Bax has been shown to be required for resection-induced apoptosis. It has also been demonstrated that p38-α MAPK (p38) is necessary for Bax activation and apoptosis in vitro. The present studies were designed to test the hypothesis that p38 is a key regulator of Bax activation during adaptation after SBR in vivo. Enterocyte expression of p38 was deleted by tamoxifen administration to activate villin-Cre in adult mice with a floxed Mapk14 (p38-α) gene. Proximal 50% SBR or sham operations were performed on wild-type (WT) and p38 intestinal knockout (p38-IKO) mice under isoflurane anesthesia. Mice were killed 3 or 7 days after operation, and adaptation was analyzed by measuring intestinal morphology, proliferation, and apoptosis. Bax activity was quantified by immunoprecipitation, followed by Western blotting. After SBR, p38-IKO mice had deeper crypts, longer villi, and accelerated proliferation compared with WT controls. Rates of crypt apoptosis were significantly lower in p38-IKO mice, both at baseline and after SBR. Levels of activated Bax were twofold higher in WT mice after SBR relative to sham. In contrast, activated Bax levels were reduced by 67% in mice after p38 MAPK deletion. Deleted p38 expression within the intestinal epithelium leads to enhanced adaptation and reduced levels of enterocyte apoptosis after massive intestinal resection. p38-regulated Bax activation appears to be an important mechanism underlying resection-induced apoptosis.

Indexed as

AnimalsApoptosisbcl-2-Associated X ProteinCells, CulturedEnterocytesIntestinesMiceMice, Knockoutp38 Mitogen-Activated Protein KinasesShort Bowel SyndromeBax protein, mousebcl-2-Associated X Proteinp38 Mitogen-Activated Protein Kinases

Identifiers

PMID22383494
PMCPMC3362074
OpenAlexW2157568265

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.