Evidence map›Paper›PMID 10066923›Full record

ArticleThe Journal of physiology1999

Role of Rho and Rho kinase in the activation of volume-regulated anion channels in bovine endothelial cells.

B Nilius, T Voets, J Prenen, H Barth, K Aktories, K Kaibuchi, G Droogmans, J Eggermont

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of physiology, 1999. 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
5.0field-weighted citation impact, top 4% 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, 142 citations in OpenAlex.

  1. Article
  2. Review
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  4. Article
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  6. Review
  7. Article
  8. Review
  9. Hypotonic swelling-induced activation of PKN1 mediates cell survival in cardiac myocytes.American journal of physiology. Heart and circulatory physiology · 2011
    Article
  10. Article
  11. Article
  12. Review
  13. Influenza A virus inhibits alveolar fluid clearance in BALB/c mice.American journal of respiratory and critical care medicine · 2008
    Article
  14. Article
  15. Article
  16. Diversity of Cl(-) channels.Cellular and molecular life sciences : CMLS · 2006
    Review
  17. Article
  18. Article
  19. Review
  20. 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

8 authors at 3 institutions in 3 countries.

B NiliusKatholieke Universiteit Leuven, Laboratorium voor Fysiologie, Campus Gasthuisberg, B-3000 Leuven, Belgium. bernd.nilius@med.kuleuven.ac.be
T Voets
J Prenen
H Barth
K Aktories
K Kaibuchi
G Droogmans
J Eggermont
KU Leuven · BEUniversity of Freiburg · DENara Institute of Science and Technology · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

1. We have studied the modulation of volume-regulated anion channels (VRACs) by the small GTPase Rho and by one of its targets, Rho kinase, in calf pulmonary artery endothelial (CPAE) cells. 2. RT-PCR and immunoblot analysis showed that both RhoA and Rho kinase are expressed in CPAE cells. 3. ICl,swell, the chloride current through VRACs, was activated by challenging CPAE cells with a 25 % hypotonic extracellular solution (HTS) or by intracellular perfusion with a pipette solution containing 100 microM GTPgammaS. 4. Pretreatment of CPAE cells with the Clostridium C2IN-C3 fusion toxin, which inactivates Rho by ADP ribosylation, significantly impaired the activation of ICl,swell in response to the HTS. The current density at +100 mV was 49 +/- 13 pA pF-1 (n = 17) in pretreated cells compared with 172 +/- 17 pA pF-1 (n = 21) in control cells. 5. The volume-independent activation of ICl,swell by intracellular perfusion with GTPgammaS was also impaired in C2IN-C3-pretreated cells (31 +/- 7 pA pF-1, n = 11) compared with non-treated cells (132 +/- 21 pA pF-1, n = 15). 6. Activation of ICl,swell was pertussis toxin (PTX) insensitive. 7. Y-27632, a blocker of Rho kinase, inhibited ICl,swell and delayed its activation. 8. Inhibition of Rho and of Rho kinase by the above-described treatments did not affect the extent of cell swelling in response to HTS. 9. These experiments provide strong evidence that the Rho-Rho kinase pathway is involved in the VRAC activation cascade.

Indexed as

GTPase-Activating ProteinsAmidesAnimalsBotulinum ToxinsCalcium ChannelsCattleCells, CulturedElectrophysiologyEndothelium, VascularEnzyme InhibitorsGTP-Binding ProteinsHypotonic SolutionsImmunoblottingIntracellular Signaling Peptides and ProteinsIon ChannelsPatch-Clamp TechniquesAmidesBotulinum Toxinsbotulinum toxin type CCalcium ChannelsEnzyme InhibitorsGTPase-Activating ProteinsGTP-Binding ProteinsHypotonic SolutionsIntracellular Signaling Peptides and ProteinsIon ChannelsPertussis ToxinProtein Serine-Threonine KinasesPyridinesrho-Associated Kinasesrho GTPase-activating proteinVirulence Factors, BordetellaY 27632

Identifiers

PMID10066923
PMCPMC2269225
OpenAlexW2001746599

What OpenQuestion holds

Texttitle and abstract
measurements read6
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.