Evidence map›Paper›PMID 30809154›Full record

ArticleFrontiers in physiology2019

KLF4-Induced Connexin40 Expression Contributes to Arterial Endothelial Quiescence.

Jean-François Denis, Mannekomba R Diagbouga, Filippo Molica, Aurélie Hautefort, Tanja Linnerz, Masakatsu Watanabe, Sylvain Lemeille, Julien Y Bertrand, Brenda R Kwak

Open access · goldAbstract read
In one paragraph

Article in Frontiers in physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

22 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Article
  3. Vascular mechanical forces and vascular diseases.Journal of advanced research · 2026
    Review
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  6. Article
  7. Review
  8. Article
  9. Article
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  13. Article
  14. The Potential Role of Connexins in the Pathogenesis of Atherosclerosis.International journal of molecular sciences · 2023
    Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
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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

9 authors at 2 institutions in 2 countries.

Jean-François DenisDepartment of Pathology and Immunology, University of Geneva, Geneva, Switzerland.
Mannekomba R DiagbougaDepartment of Pathology and Immunology, University of Geneva, Geneva, Switzerland.
Filippo MolicaDepartment of Pathology and Immunology, University of Geneva, Geneva, Switzerland.
Aurélie HautefortDepartment of Pathology and Immunology, University of Geneva, Geneva, Switzerland.
Tanja LinnerzDepartment of Pathology and Immunology, University of Geneva, Geneva, Switzerland.
Masakatsu WatanabeGraduate School of Frontier Biosciences, Osaka University, Osaka, Japan.
Sylvain LemeilleDepartment of Pathology and Immunology, University of Geneva, Geneva, Switzerland.
Julien Y BertrandDepartment of Pathology and Immunology, University of Geneva, Geneva, Switzerland.
Brenda R KwakDepartment of Pathology and Immunology, University of Geneva, Geneva, Switzerland.
University of Geneva · CHUbe Frontier University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Shear stress, a blood flow-induced frictional force, is essential in the control of endothelial cell (EC) homeostasis. High laminar shear stress (HLSS), as observed in straight parts of arteries, assures a quiescent non-activated endothelium through the induction of Krüppel-like transcription factors (KLFs). Connexin40 (Cx40)-mediated gap junctional communication is known to contribute to a healthy endothelium by propagating anti-inflammatory signals between ECs, however, the molecular basis of the transcriptional regulation of Cx40 as well as its downstream effectors remain poorly understood. Here, we show that flow-induced KLF4 regulated Cx40 expression in a mouse EC line. Chromatin immunoprecipitation in ECs revealed that KLF4 bound to three predicted KLF consensus binding sites in the Cx40 promoter. HLSS-dependent induction of Cx40 expression was confirmed in primary human ECs. The downstream effects of Cx40 modulation in ECs exposed to HLSS were elucidated by an unbiased transcriptomics approach. Cell cycle progression was identified as an important downstream target of Cx40 under HLSS. In agreement, an increase in the proportion of proliferating cell nuclear antigen (PCNA)-positive ECs and a decrease in the proportion of ECs in the G0/G1 phase were observed under HLSS after Cx40 silencing. Transfection of communication-incompetent HeLa cells with Cx40 demonstrated that the regulation of proliferation by Cx40 was not limited to ECs. Using a zebrafish model, we finally showed faster intersegmental vessel growth and branching into the dorsal longitudinal anastomotic vessel in embryos knock-out for the Cx40 orthologs

Indexed as

cell proliferationCx40endotheliumKLF4shear stress

Identifiers

PMID30809154
PMCPMC6379456
OpenAlexW2914257008

What OpenQuestion holds

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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.