Evidence map›Paper›PMID 19179620›Full record

ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2009

Delineating the signals by which repetitive deformation stimulates intestinal epithelial migration across fibronectin.

Christopher P Gayer, Lakshmi S Chaturvedi, Shouye Wang, Brittany Alston, Thomas L Flanigan, Marc D Basson

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Gastrointestinal and liver physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

13 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Loss of MLK3 signaling impedes ulcer healing by modulating MAPK signaling in mouse intestinal mucosa.American journal of physiology. Gastrointestinal and liver physiology · 2012
    Article
  8. Recent advances in small bowel diseases: Part I.World journal of gastroenterology · 2012
    Review
  9. Article
  10. ILK mediates the effects of strain on intestinal epithelial wound closure.American journal of physiology. Cell physiology · 2011
    Article
  11. Schlafen 3 induction by cyclic strain regulates intestinal epithelial differentiation.American journal of physiology. Gastrointestinal and liver physiology · 2010
    Article
  12. Article
  13. 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

6 authors at 1 institution in 1 country.

Christopher P GayerDepartment of Surgery, John D. Dingell VA Medical Center, Wayne State University, Detroit, MI, USA.
Lakshmi S Chaturvedi
Shouye Wang
Brittany Alston
Thomas L Flanigan
Marc D Basson
John D. Dingell VA Medical Center · US

Funding

Regulation of FAK protein in mucosal healingR01DK067257 · NIDDK · WAYNE STATE UNIVERSITY · PI BASSON, MARC D. · 2005 to 2009
$1.2M
ACADEMIC TRAINING IN TRAUMA AND BURNST32GM008420 · NIGMS · WAYNE STATE UNIVERSITY · PI BASSON, MARC D. · 1992 to 2009
$1.2M
NIDDK NIH HHS R01 DK067257NIGMS NIH HHS 2 T32 GM008420
6 · The paper itself

Abstract

Repetitive strain stimulates intestinal epithelial migration across fibronectin via focal adhesion kinase (FAK), Src, and extracellular signal-related kinase (ERK) although how these signals act and interact remains unclear. We hypothesized that PI3K is central to this pathway. We subjected Caco-2 and intestinal epithelial cell-6 cells to 10 cycles/min deformation on flexible fibronectin-coated membranes, assayed migration by wound closure, and signaling by immunoblots. Strain stimulated PI3K, AKT, glycogen synthase kinase (GSK), and p38 phosphorylation. Blocking each kinase prevented strain stimulation of migration. Blocking PI3K prevented strain-stimulated ERK and p38 phosphorylation. Blocking AKT did not. Downstream, blocking PI3K, AKT, or ERK inhibited strain-induced GSK-Ser9 phosphorylation. Upstream of AKT, reducing FAK or Rac1 by siRNA blocked strain-stimulated AKT phosphorylation, but inhibiting Src by PP2 or siRNA did not. Transfection with FAK point mutants at Tyr397, Tyr576/577, or Tyr925 demonstrated that only FAK925 phosphorylation is required for strain-stimulated AKT phosphorylation. Myosin light chain activation by strain required FAK, Rac1, PI3K, AKT, GSK, and ERK but not Src or p38. Finally, blebbistatin, a nonmuscle myosin II inhibitor, blocked the motogenic effect of strain downstream of myosin light chain. Thus strain stimulates intestinal epithelial migration across fibronectin by a complex pathway including Src, FAK, Rac1, PI3K, AKT, GSK, ERK, p38, myosin light chain, and myosin II.

Indexed as

AnimalsCell LineCell MovementEpithelial CellsFibronectinsFocal Adhesion Protein-Tyrosine KinasesGlycogen Synthase KinasesHumansIntestinal MucosaMechanotransduction, Cellularp38 Mitogen-Activated Protein KinasesPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsPhosphorylationProto-Oncogene Proteins c-aktRatsFibronectinsFocal Adhesion Protein-Tyrosine KinasesGlycogen Synthase Kinasesp38 Mitogen-Activated Protein KinasesPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsProto-Oncogene Proteins c-akt

Identifiers

PMID19179620
PMCPMC2670672
OpenAlexW2149511051

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.