Evidence map›Paper›PMID 31681446›Full record

ArticleCellular and molecular bioengineering2019

The TRPV4-TAZ mechanotransduction signaling axis in matrix stiffness- and TGFβ1-induced epithelial-mesenchymal transition.

Shweta Sharma, Rishov Goswami, Shaik O Rahaman

Abstract read
In one paragraph

Article in Cellular and molecular bioengineering, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing 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

34 citing papers in PubMed.

  1. A novel role for TRPV1 in macrophage giant cell formation.bioRxiv : the preprint server for biology · 2026
    Article
  2. Review
  3. Review
  4. TRPV4-Mediated Mechanosensing Regulates the Endothelial-to-Mesenchymal Transition: Implications for Atherosclerosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. YAP/TAZ Signalling Controls Epidermal Keratinocyte Fate.International journal of molecular sciences · 2024
    Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. CaCellular signalling · 2023
    Review
  17. Article
  18. Article
  19. Article
  20. Hydrogel cultures reveal Transient Receptor Potential Vanilloid 4 regulation of myofibroblast activation and proliferation in valvular interstitial cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022
    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.

Shweta SharmaDepartment of Nutrition and Food Science, University of Maryland, College Park, MD 20742 USA.
Rishov GoswamiDepartment of Nutrition and Food Science, University of Maryland, College Park, MD 20742 USA.
Shaik O RahamanDepartment of Nutrition and Food Science, University of Maryland, College Park, MD 20742 USA.

Funding

Role of TRPV4 mechanotransduction in foreign body responseR01EB024556 · NIBIB · UNIV OF MARYLAND, COLLEGE PARK · PI RAHAMAN, SHAIK O, ZHU, XIAOPING · 2017 to 2020
$1.7M
NIBIB NIH HHS R01 EB024556
6 · The paper itself

Abstract

introductionThe implantation of biomaterials into soft tissue leads to the development of foreign body response, a non-specific inflammatory condition that is characterized by the presence of fibrotic tissue. Epithelial-mesenchymal transition (EMT) is a key event in development, fibrosis, and oncogenesis. Emerging data support a role for both a mechanical signal and a biochemical signal in EMT. We hypothesized that transient receptor potential vanilloid 4 (TRPV4), a mechanosensitive channel, is a mediator of EMT.

methodsNormal human primary epidermal keratinocytes (NHEKs) were seeded on collagen-coated plastic plates or varied stiffness polyacrylamide gels in the presence or absence of TGFβ1, Immunofluorescence, immunoblot, and polymerase chain reaction analysis were performed to determine expression level of EMT markers and signaling proteins. Knock-down of TRPV4 function was achieved by siRNA transfection or by GSK2193874 treatment.

resultsWe found that knock-down of TRPV4 blocked both matrix stiffness- and TGFβ1-induced EMT in NHEKs. In a murine skin fibrosis model, TRPV4 deletion resulted in decreased expression of the mesenchymal marker, α-SMA, and increased expression of epithelial marker, E-cadherin. Mechanistically, our data showed that: i) TRPV4 was essential for the nuclear translocation of TAZ in response to matrix stiffness and TGFβ1; ii) Antagonism of TRPV4 inhibited both matrix stiffness-induced and TGFβ1-induced expression of TAZ proteins; and iii) TRPV4 antagonism suppressed both matrix stiffness-induced and TGFβ1-induced activation of Smad2/3, but not of AKT.

conclusionsThese data identify a novel role for TRPV4-TAZ mechanotransduction signaling axis in regulating EMT in NHEKs in response to both matrix stiffness and TGFβ1.

Indexed as

epithelial-mesenchymal transitionfibrosiskeratinocytesmatrix stiffnessSmad2/3TAZTRPV4

Identifiers

PMID31681446
PMCPMC6816769

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Registered trials

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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.