Evidence map›Paper›PMID 18667438›Full record

ArticleThe Journal of biological chemistry2008

RhoA GTPase and F-actin dynamically regulate the permeability of Cx43-made channels in rat cardiac myocytes.

Mickaël Derangeon, Nicolas Bourmeyster, Isabelle Plaisance, Caroline Pinet-Charvet, Qian Chen, Fabien Duthe, Michel R Popoff, Denis Sarrouilhe, Jean-Claude Hervé

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

23 citing papers in PubMed, 48 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. RhoA/ROCK Regulates Prion Pathogenesis by Controlling Connexin 43 Activity.International journal of molecular sciences · 2020
    Article
  7. Gap Junctions and Wnt Signaling in the Mammary Gland: a Cross-Talk?Journal of mammary gland biology and neoplasia · 2019
    Review
  8. Intracellular CaInternational journal of molecular sciences · 2018
    Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Modulation of connexin signaling by bacterial pathogens and their toxins.Cellular and molecular life sciences : CMLS · 2011
    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

9 authors at 2 institutions in 1 country.

Mickaël DerangeonInstitut de Physiologie et Biologie Cellulaires, Université de Poitiers, F-86022 Poitiers, France.
Nicolas Bourmeyster
Isabelle Plaisance
Caroline Pinet-Charvet
Qian Chen
Fabien Duthe
Michel R Popoff
Denis Sarrouilhe
Jean-Claude Hervé
Université de Poitiers · FRInstitut Pasteur · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gap junctions are clusters of transmembrane channels allowing a passive diffusion of ions and small molecules between adjacent cells. Connexin43, the main channel-forming protein expressed in ventricular myocytes, can associate with zonula occludens-1, a scaffolding protein linked to the actin cytoskeleton and to signal transduction molecules. The possible influence of Rho GTPases, major regulators of cellular junctions and of the actin cytoskeleton, in the modulation of gap junctional intercellular communication (GJIC) was examined. The activation of RhoA by cytoxic necrotizing factor 1 markedly enhanced GJIC, whereas its specific inhibition by the Clostridium botulinum C3 exoenzyme significantly reduced it. RhoA activity affects GJIC without major cellular redistribution of junctional plaques or changes in the Cx43 phosphorylation pattern. As these GTPases frequently act via the cortical cytoskeleton, the importance of F-actin in the modulation of GJIC was investigated by means of agents interfering with actin polymerization. Cytoskeleton stabilization by phalloidin slowed down the kinetics of channel rundown in the absence of ATP, whereas its disruption by cytochalasin D rapidly and markedly reduced GJIC despite ATP presence. Cytoskeleton stabilization by phalloidin markedly reduced the consequences of RhoA activation or inactivation. This mechanism appears to be the first described capable to both up- or down-regulate GJIC through RhoA activation or, conversely, inhibition. The inhibition of Rho downstream kinase effectors had no effect on GJIC. The present results provide further insight into the gating and regulation of junctional channels and identify a new downstream target for the small G-protein RhoA.

Indexed as

ActinsAdenosine TriphosphateADP Ribose TransferasesAnimalsBacterial ToxinsBotulinum ToxinsCell Membrane PermeabilityConnexin 43Cytochalasin DCytoskeletonEnzyme ActivationEscherichia coli ProteinsGap JunctionsKineticsMembrane ProteinsMyocytes, CardiacActinsAdenosine TriphosphateADP Ribose TransferasesBacterial ToxinsBotulinum ToxinsConnexin 43Cytochalasin Dcytotoxic necrotizing factor type 1Escherichia coli Proteinsexoenzyme C3, Clostridium botulinumMembrane ProteinsNucleic Acid Synthesis InhibitorsPhalloidinePhosphoproteinsPoisonsrhoA GTP-Binding ProteinTjp1 protein, ratZonula Occludens-1 Protein

Identifiers

PMID18667438
PMCPMC2662158
OpenAlexW1979891440

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.