Evidence map›Paper›PMID 25616899›Full record

ArticleJournal of cell science2015

Hypoxia increases the abundance but not the assembly of extracellular fibronectin during epithelial cell transdifferentiation.

Manish K Rana, Jyoti Srivastava, Michael Yang, Christopher S Chen, Diane L Barber

Open access · bronzeAbstract read
In one paragraph

Article in Journal of cell science, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.2field-weighted citation impact, top 20% 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

18 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Hypoxia-induced blood-brain barrier dysfunction is prevented by pericyte-conditioned media via attenuated actomyosin contractility and claudin-5 stabilization.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022
    Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. HIF-hypoxia signaling in skeletal muscle physiology and fibrosis.Journal of cell communication and signaling · 2020
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. 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 3 institutions in 1 country.

Manish K RanaDepartment of Cell and Tissue Biology, University of California, San Francisco, CA 94143, USA Department of Biomedical Engineering, Boston University and Wyss Institute for Biologically Inspired Engineering, Harvard University, Boston, MA 02215, USA.
Jyoti SrivastavaDepartment of Cell and Tissue Biology, University of California, San Francisco, CA 94143, USA.
Michael YangDepartment of Biomedical Engineering, Boston University and Wyss Institute for Biologically Inspired Engineering, Harvard University, Boston, MA 02215, USA.
Christopher S ChenDepartment of Biomedical Engineering, Boston University and Wyss Institute for Biologically Inspired Engineering, Harvard University, Boston, MA 02215, USA.
Diane L BarberDepartment of Cell and Tissue Biology, University of California, San Francisco, CA 94143, USA diane.barber@ucsf.edu.
Harvard University · USUniversity of California, San Francisco · USBoston University · US

Funding

MECHANISMS OF RECEPTOR-REGULATED NA+/H+ EXCHANGER01GM047413 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI BARBER, DIANE L · 1993 to 2014
$4.2M
Spinning disk confocal / FRAP microscope for quantitative live cell imagingS10RR026758 · NCRR · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI WITTMANN, TORSTEN · 2010 to 2010
$500k
NCRR NIH HHS S10 RR026758NIGMS NIH HHS GM47413NIGMS NIH HHS R01 GM047413
6 · The paper itself

Abstract

Increased production and assembly of extracellular matrix proteins during transdifferentiation of epithelial cells to a mesenchymal phenotype contributes to diseases such as renal and pulmonary fibrosis. TGF-β and hypoxia, two cues that initiate injury-induced fibrosis, caused human kidney cells to develop a mesenchymal phenotype, including increased fibronectin expression and secretion. However, upon hypoxia, assembled extracellular fibronectin fibrils were mostly absent, whereas treatment with TGF-β led to abundant fibrils. Fibrillogenesis required cell-generated force and tension. TGF-β, but not hypoxia, increased cell contractility, as determined by phosphorylation of myosin light chain and quantifying force and tension generated by cells plated on engineered elastomeric microposts. Additionally, TGF-β, but not hypoxia, increased the activation of integrins. However, experimentally activating integrins markedly increased the levels of phosphorylated myosin light chain and fibronectin fibril assembly upon hypoxia. Our findings show that deficient integrin activation and subsequent lack of cell contractility are mechanisms that mediate a lack of fibrillogenesis upon hypoxia and they challenge current views on oxygen deprivation being sufficient for fibrosis.

Indexed as

Cell TransdifferentiationBlotting, WesternCells, CulturedEpithelial CellsExtracellular MatrixFibronectinsFibrosisHumansHypoxiaIntegrinsKidney Tubules, ProximalTransforming Growth Factor betaFibronectinsIntegrinsTransforming Growth Factor betaExtracellular matrixFibronectinFibrosisHypoxiaTGF-β

Identifiers

PMID25616899
PMCPMC4359919
OpenAlexW2319798473

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.