Evidence map›Paper›PMID 22421965›Full record

ArticleCell death and differentiation2012

Actin reorganization as the molecular basis for the regulation of apoptosis in gastrointestinal epithelial cells.

Y Wang, S P George, K Srinivasan, S Patnaik, S Khurana

Open access · bronzeAbstract read
In one paragraph

Article in Cell death and differentiation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.7field-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

16 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Review
  3. Regulation of Mitochondrial Function by the Actin Cytoskeleton.Frontiers in cell and developmental biology · 2021
    Review
  4. Loss of Slfn3 induces a sex-dependent repair vulnerability after 50% bowel resection.American journal of physiology. Gastrointestinal and liver physiology · 2021
    Article
  5. Review
  6. Article
  7. Involvement of the Actin Machinery in Programmed Cell Death.Frontiers in cell and developmental biology · 2020
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
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

5 authors at 3 institutions in 1 country.

Y WangThe Department of Physiology, The University of Tennessee Health Science Center, Memphis, TN 38163, USA.
S P George
K Srinivasan
S Patnaik
S Khurana
University of Houston · USUniversity of Tennessee Health Science Center · USVanderbilt University · US

Funding

Tissue Analysis & Molecular Imaging CoreP30DK056338 · NIDDK · BAYLOR COLLEGE OF MEDICINE · PI Geoffrey A Preidis · 2001 to 2026
$28.3M
ROLE OF VILLIN IN EPITHELIAL CELL SIGNAL TRANSDUCTIONR01DK054755 · NIDDK · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI KHURANA, SEEMA · 2000 to 2009
$3.1M
Regulation of epithelial cell motility by villin.R01DK065006 · NIDDK · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI KHURANA, SEEMA · 2004 to 2008
$1.6M
Regulation of epithelial cell homeostasis by actin microfilamentsR01DK081408 · NIDDK · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI KHURANA, SEEMA · 2009 to 2010
$785k
NIDDK NIH HHS DK-54755NIDDK NIH HHS DK56338NIDDK NIH HHS DK-65006NIDDK NIH HHS DK-81408NIDDK NIH HHS P30 DK056338NIDDK NIH HHS R01 DK054755NIDDK NIH HHS R01 DK065006NIDDK NIH HHS R01 DK081408
6 · The paper itself

Abstract

The gastrointestinal (GI) epithelium is a rapidly renewing tissue in which apoptosis represents part of the overall homeostatic process. Regulation of apoptosis in the GI epithelium is complex with a precise relationship between cell position and apoptosis. Apoptosis occurs spontaneously and in response to radiation and cytotoxic drugs at the base of the crypts. By contrast, the villus epithelial cells are extremely resistant to apoptosis. The molecular mechanism underlying this loss of function of villus epithelial cells to undergo apoptosis shortly after their exit from the crypt is unknown. In this study we demonstrate for the first time, that deletion of two homologous actin-binding proteins, villin and gelsolin renders villus epithelial cells extremely sensitive to apoptosis. Ultrastructural analysis of the villin-gelsolin(-/-) double-knockout mice shows an abnormal accumulation of damaged mitochondria demonstrating that villin and gelsolin function on an early step in the apoptotic signaling at the level of the mitochondria. A characterization of functional and ligand-binding mutants demonstrate that regulated changes in actin dynamics determined by the actin severing activities of villin and gelsolin are required to maintain cellular homeostasis. Our study provides a molecular basis for the regulation of apoptosis in the GI epithelium and identifies cell biological mechanisms that couple changes in actin dynamics to apoptotic cell death.

Indexed as

ActinsAnimalsApoptosisEpithelial CellsGastric MucosaGelsolinIntestinal MucosaMiceMice, KnockoutMicrofilament ProteinsMitochondriaActinsGelsolinMicrofilament Proteinsvillin

Identifiers

PMID22421965
PMCPMC3422475
OpenAlexW2076918427

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.