Evidence map›Paper›PMID 10198070›Full record

ArticleMolecular biology of the cell1999

Temporary disruption of the plasma membrane is required for c-fos expression in response to mechanical stress.

K P Grembowicz, D Sprague, P L McNeil

Abstract read
In one paragraph

Article in Molecular biology of the cell, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing 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

35 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
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  5. Article
  6. Article
  7. Review
  8. Computational and structural biotechnology journal · 2021
    Article
  9. Article
  10. Using tools in mechanobiology to repair tendons.Current tissue microenvironment reports · 2020
    Article
  11. Article
  12. Review
  13. Review
  14. Mechanical loading disrupts osteocyte plasma membranes which initiates mechanosensation events in bone.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2018
    Article
  15. Article
  16. Article
  17. Article
  18. Biophysical determinants of alveolar epithelial plasma membrane wounding associated with mechanical ventilation.American journal of physiology. Lung cellular and molecular physiology · 2013
    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

3 authors.

K P GrembowiczInstitute of Molecular Medicine and Genetics, Department of Cellular Biology and Anatomy, Medical College of Georgia, Augusta, GA, 30912-2000, USA.
D Sprague
P L McNeil

Funding

PHS HHS NIH 48091
6 · The paper itself

Abstract

Mechanically stressed cells display increased levels of fos message and protein. Although the intracellular signaling pathways responsible for FOS induction have been extensively characterized, we still do not understand the nature of the primary cell mechanotransduction event responsible for converting an externally acting mechanical stressor into an intracellular signal cascade. We now report that plasma membrane disruption (PMD) is quantitatively correlated on a cell-by-cell basis with fos protein levels expressed in mechanically injured monolayers. When the population of PMD-affected cells in injured monolayers was selectively prevented from responding to the injury, the fos response was completely ablated, demonstrating that PMD is a requisite event. This PMD-dependent expression of fos protein did not require cell exposure to cues inherent in release from cell-cell contact inhibition or presented by denuded substratum, because it also occurred in subconfluent monolayers. Fos expression also could not be explained by factors released through PMD, because cell injury conditioned medium failed to elicit fos expression. Translocation of the transcription factor NF-kappaB into the nucleus may also be regulated by PMD, based on a quantitative correlation similar to that found with fos. We propose that PMD, by allowing a flux of normally impermeant molecules across the plasma membrane, mediates a previously unrecognized form of cell mechanotransduction. PMD may thereby lead to cell growth or hypertrophy responses such as those that are present normally in mechanically stressed skeletal muscle and pathologically in the cardiovascular system.

Indexed as

Gene Expression RegulationGenes, fos3T3 CellsAnimalsAortaCattleCell MembraneCells, CulturedCulture Media, ConditionedEndothelium, VascularKineticsMiceModels, BiologicalProtein BiosynthesisProto-Oncogene Proteins c-fosRegression AnalysisCulture Media, ConditionedProto-Oncogene Proteins c-fosRNA, Messenger

Identifiers

PMID10198070
PMCPMC25264

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.