Evidence map›Paper›PMID 21257731›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2011

Endocytic response of type I alveolar epithelial cells to hypertonic stress.

Shaohua Wang, Raman Deep Singh, Lindsay Godin, Richard E Pagano, Rolf D Hubmayr

Abstract read
In one paragraph

Article in American journal of physiology. Lung cellular and molecular physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
–field-weighted citation impact
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

26 citing papers in PubMed.

  1. Aging-Associated Molecular Changes in Human Alveolar Type I Cells.Journal of respiratory biology and translational medicine · 2024
    Article
  2. Article
  3. Article
  4. Article
  5. Lysosomal solute and water transport.The Journal of cell biology · 2022
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Inhaled TRIM72 Protein Protects Ventilation Injury to the Lung through Injury-guided Cell Repair.American journal of respiratory cell and molecular biology · 2018
    Article
  16. Article
  17. Plasma membrane wounding and repair in pulmonary diseases.American journal of physiology. Lung cellular and molecular physiology · 2017
    Review
  18. TRIM72 modulates caveolar endocytosis in repair of lung cells.American journal of physiology. Lung cellular and molecular physiology · 2016
    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.

Shaohua WangThoracic Diseases Research Unit, Division of Pulmonary and Critical Care Medicine, Department of Medicine, Mayo Clinic, Rochester, Minnesota, USA.
Raman Deep Singh
Lindsay Godin
Richard E Pagano
Rolf D Hubmayr

Funding

INTRACELLULAR TRANSLOCATION AND METABOLISM OF LIPIDSR01GM022942 · NIGMS · MAYO CLINIC ROCHESTER · PI MARKS, DAVID LARRY · 1985 to 2010
$5.3M
MECHANICS AND DEFORMATION RESPONSES OF LUNG CELLSR01HL063178 · NHLBI · MAYO CLINIC ROCHESTER · PI HUBMAYR, ROLF D · 2000 to 2011
$4.2M
MEMBRANE TRAFFIC IN SPHINGOLIPID STORAGE DISEASESR01GM060934 · NIGMS · MAYO CLINIC ROCHESTER · PI LIMPER, ANDREW H · 2001 to 2011
$2.9M
INTRACELLULAR TRANSLOCATION AND METABOLISM OF LIPIDSR37GM022942 · NIGMS · MAYO CLINIC COLL OF MEDICINE, ROCHESTER · PI PAGANO, RICHARD E · 1989 to 1998
–
NHLBI NIH HHS HL 63178NIGMS NIH HHS GM 22942NIGMS NIH HHS GM 60934
6 · The paper itself

Abstract

We present plasma membrane (PM) internalization responses of type I alveolar epithelial cells to a 50 mosmol/l increase in tonicity. Our research is motivated by interest in ATI repair, for which endocytic retrieval of PM appears to be critical. We validated pharmacological and molecular tools to dissect the endocytic machinery of these cells and used these tools to test the hypothesis that osmotic stress triggers a pathway-specific internalization of PM domains. Validation experiments confirmed the fluorescent analogs of lactosyl-ceramide, transferrin, and dextran as pathway-specific cargo of caveolar, clathrin, and fluid-phase uptake, respectively. Pulse-chase experiments indicate that hypertonic exposure causes a downregulation of clathrin and fluid-phase endocytosis while stimulating caveolar endocytosis. The tonicity-mediated increase in caveolar endocytosis was associated with the translocation of caveolin-1 from the PM and was absent in cells that had been transfected with dominant-negative dynamin constructs. In separate experiments we show that hypertonic exposure increases the probability of PM wound repair following micropuncture from 82 ± 4 to 94 ± 2% (P < 0.01) and that this effect depends on Src pathway activation-mediated caveolar endocytosis. The therapeutic and biological implications of our findings are discussed.

Indexed as

Alveolar Epithelial CellsAnimalsAntigens, CDCaveolin 1Cell MembraneClathrinDextransEndocytosisEnzyme ActivationGenes, DominantHypertonic SolutionsLactosylceramidesOsmotic PressurePuncturesRatsSignal TransductionAntigens, CDCaveolin 1CDw17 antigenClathrinDextransHypertonic SolutionsLactosylceramidessrc-Family KinasesTransferrin

Identifiers

PMID21257731
PMCPMC3075106

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.