Evidence map›Paper›PMID 22037358›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2012

PTEN inhibition improves wound healing in lung epithelia through changes in cellular mechanics that enhance migration.

Cosmin Mihai, Shengying Bao, Ju-Ping Lai, Samir N Ghadiali, Daren L Knoell

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Lung cellular and molecular physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 13% 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, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Spatiotemporal distribution of PTEN before directed cell migration in monolayers.In vitro cellular & developmental biology. Animal · 2024
    Article
  4. Article
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  8. Cytokeratin profile and keratinocyte gene expression in keratinized lid margins of patients with chronic Stevens-Johnson syndrome.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2022
    Article
  9. Article
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  11. Review
  12. Article
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  15. Article
  16. PTEN Inhibition in Human Disease Therapy.Molecules (Basel, Switzerland) · 2018
    Review
  17. Review
  18. Region-specific role for Pten in maintenance of epithelial phenotype and integrity.American journal of physiology. Lung cellular and molecular physiology · 2017
    Article
  19. Article
  20. 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

5 authors at 1 institution in 1 country.

Cosmin MihaiDepartment of Biomedical Engineering, Division of Pulmonary, Allergy, Critical Care and Sleep Medicine, The Ohio State University, Columbus, Ohio 43210, USA.
Shengying Bao
Ju-Ping Lai
Samir N Ghadiali
Daren L Knoell
The Ohio State University · US

Funding

The cytoprotective role of zinc transporters in human lung epitheliaR01HL086981 · NHLBI · OHIO STATE UNIVERSITY · PI KNOELL, DAREN LEE · 2007 to 2011
$1.9M
NHLBI NIH HHS R01 HL086981-01
6 · The paper itself

Abstract

The phosphoinositide-3 kinase/Akt pathway is a vital survival axis in lung epithelia. We previously reported that inhibition of phosphatase and tensin homolog deleted on chromosome 10 (PTEN), a major suppressor of this pathway, results in enhanced wound repair following injury. However, the precise cellular and biomechanical mechanisms responsible for increased wound repair during PTEN inhibition are not yet well established. Using primary human lung epithelia and a related lung epithelial cell line, we first determined whether changes in migration or proliferation account for wound closure. Strikingly, we observed that cell migration accounts for the majority of wound recovery following PTEN inhibition in conjunction with activation of the Akt and ERK signaling pathways. We then used fluorescence and atomic force microscopy to investigate how PTEN inhibition alters the cytoskeletal and mechanical properties of the epithelial cell. PTEN inhibition did not significantly alter cytoskeletal structure but did result in large spatial variations in cell stiffness and in particular a decrease in cell stiffness near the wound edge. Biomechanical changes, as well as migration rates, were mediated by both the Akt and ERK pathways. Our results indicate that PTEN inhibition rapidly alters biochemical signaling events that in turn provoke alterations in biomechanical properties that enhance cell migration. Specifically, the reduced stiffness of PTEN-inhibited cells promotes larger deformations, resulting in a more migratory phenotype. We therefore conclude that increased wound closure consequent to PTEN inhibition occurs through enhancement of cell migration that is due to specific changes in the biomechanical properties of the cell.

Indexed as

Actin CytoskeletonBiomechanical PhenomenaCell LineCell MovementCell ProliferationElectric ImpedanceEpithelial CellsExtracellular Signal-Regulated MAP KinasesHumansLungLung InjuryMAP Kinase Signaling SystemMicroscopy, Atomic ForcePhosphorylationProto-Oncogene Proteins c-aktPTEN PhosphohydrolasebisperoxovanadiumExtracellular Signal-Regulated MAP KinasesProto-Oncogene Proteins c-aktPTEN PhosphohydrolasePTEN protein, humanVanadium Compounds

Identifiers

PMID22037358
PMCPMC3289272
OpenAlexW2149240358

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.