Evidence map›Paper›PMID 28733642›Full record

ArticleScientific reports2017

Gap junction-mediated regulation of endothelial cellular stiffness.

Takayuki Okamoto, Eiji Kawamoto, Yoshimi Takagi, Nobuyuki Akita, Tatsuya Hayashi, Eun Jeong Park, Koji Suzuki, Motomu Shimaoka

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

33 citing papers in PubMed, 54 citations in OpenAlex.

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  6. Noncanonical functions of adhesion proteins in inflammation.American journal of physiology. Cell physiology · 2024
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  12. The Potential Role of Connexins in the Pathogenesis of Atherosclerosis.International journal of molecular sciences · 2023
    Review
  13. Connexins in endothelial cells as a therapeutic target for solid organ transplantation.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2022
    Review
  14. Article
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  20. P53 in the impaired lungs.DNA repair · 2020
    Review
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

8 authors at 5 institutions in 1 country.

Takayuki OkamotoDepartment of Pharmacology, Faculty of Medicine, Shimane University, 89-1 Enya-cho, Izumo-city, Shimane, 693-8501, Japan. okamoto@med.shimane-u.ac.jp.
Eiji KawamotoDepartment of Molecular Pathobiology and Cell Adhesion Biology, Mie University Graduate School of Medicine, 2-174 Edobashi, Tsu-city, Mie, 514-8507, Japan.
Yoshimi TakagiDepartment of Molecular Pathobiology and Cell Adhesion Biology, Mie University Graduate School of Medicine, 2-174 Edobashi, Tsu-city, Mie, 514-8507, Japan.
Nobuyuki AkitaFaculty of Medical Engineering, Suzuka University of Medical Science, 1001-1, Kishioka-cho, Suzuka-city, Mie, 510-0293, Japan.
Tatsuya HayashiDepartment of Biochemistry, Mie Prefectural College of Nursing, 1-1-1 Yumegaoka, Tsu-city, Mie, 514-0116, Japan.
Eun Jeong ParkDepartment of Molecular Pathobiology and Cell Adhesion Biology, Mie University Graduate School of Medicine, 2-174 Edobashi, Tsu-city, Mie, 514-8507, Japan.
Koji SuzukiFaculty of Pharmaceutical Science, Suzuka University of Medical Science, 3500-3, Minamitamagaki-cho, Suzuka-city, Mie, 513-8679, Japan.
Motomu ShimaokaDepartment of Molecular Pathobiology and Cell Adhesion Biology, Mie University Graduate School of Medicine, 2-174 Edobashi, Tsu-city, Mie, 514-8507, Japan. shimaoka@doc.medic.mie-u.ac.jp.
Mie University · JPSuzuka University of Medical Science · JPMie Prefectural College Of Nursing · JPMie University Hospital · JPShimane University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endothelial monolayers have shown the ability to signal each other through gap junctions. Gap junction-mediated cell-cell interactions have been implicated in the modulation of endothelial cell functions during vascular inflammation. Inflammatory mediators alter the mechanical properties of endothelial cells, although the exact role of gap junctions in this process remains unclear. Here, we sought to study the role of gap junctions in the regulation of endothelial stiffness, an important physical feature that is associated with many vascular pathologies. The endothelial cellular stiffness of living endothelial cells was determined by using atomic force microscopy. We found that tumor necrosis factor-α transiently increased endothelial cellular stiffness, which is regulated by cytoskeletal rearrangement and cell-cell interactions. We explored the role of gap junctions in endothelial cellular stiffening by utilizing gap junction blockers, carbenoxolone, inhibitory anti-connexin 32 antibody or anti-connexin 43 antibody. Blockade of gap junctions induced the cellular stiffening associated with focal adhesion formation and cytoskeletal rearrangement, and prolonged tumor necrosis factor-α-induced endothelial cellular stiffening. These results suggest that gap junction-mediated cell-cell interactions play an important role in the regulation of endothelial cellular stiffness.

Indexed as

ActinsCell CommunicationCell PlasticityCells, CulturedEndothelial CellsFocal AdhesionsGap JunctionsHumansHuman Umbilical Vein Endothelial CellsMicroscopy, Atomic ForceTumor Necrosis Factor-alphaVinculinActinsTumor Necrosis Factor-alphaVCL protein, humanVinculin

Identifiers

PMID28733642
PMCPMC5522438
OpenAlexW2736268164

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.