Evidence map›Paper›PMID 12937294›Full record

ArticleThe Journal of physiology2003

Modulation of Ca2+-dependent Cl- channels by calcineurin in rabbit coronary arterial myocytes.

Jonathan Ledoux, Iain Greenwood, Louis R Villeneuve, Normand Leblanc

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

15 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Molecular mechanism of TMEM16A regulation: role of CaMKII and PP1/PP2A.American journal of physiology. Cell physiology · 2019
    Article
  6. Article
  7. Vascular CaMKII: heart and brain in your arteries.American journal of physiology. Cell physiology · 2016
    Review
  8. Article
  9. Review
  10. Calcineurin-dependent ion channel regulation in heart.Trends in cardiovascular medicine · 2014
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. 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

4 authors at 3 institutions in 3 countries.

Jonathan LedouxDepartment of Physiology, University of Montréal and Research Centre, Montréal Heart Institute, Montréal, Québec, Canada.
Iain Greenwood
Louis R Villeneuve
Normand Leblanc
Université de Montréal · CASt George's, University of London · GBUniversity of Nevada, Reno · US

Funding

Wellcome Trust
6 · The paper itself

Abstract

The role of the Ca2+-dependent phosphatase calcineurin (CaN) in the modulation of Ca2+-dependent Cl- channels (ClCa) was studied in freshly isolated rabbit coronary arterial myocytes. Immunocytochemical experiments showed that calmodulin-dependent protein kinase II (CaMKII) and CaN were distributed evenly throughout the cytoplasm of coronary myocytes at rest and translocated to the plasmalemma when intracellular Ca2+ was increased. ClCa currents (ICl(Ca)) elicited by cell dialysis with fixed intracellular Ca2+ levels up to 500 nM were inhibited by 10 microM cyclosporin A (CsA), a specific inhibitor of CaN, in a voltage-dependent manner, whereas currents evoked by 1 microM Ca2+ were not affected. Inhibition of CaN with CsA also led to a significant reduction in Ca2+ sensitivity of the channel at +50 mV; half-maximal activation increased from 363 +/- 16 nM Ca2+ in control to 515 +/- 40 nM Ca2+ in the presence of CsA. Similar effects were observed on ICl(Ca) when a specific peptide fragment inhibitor of CaN (CaN-AF, 5 microM) was dialysed into the cell via the pipette (500 nM Ca2+). Application of KN-93 (10 microM), a specific inhibitor of CaMKII, enhanced ICl(Ca) in myocytes dialysed with 1 microM Ca2+ but produced no significant effect on this current when the cells were dialysed with 350 or 500 nM Ca2+. These results are consistent with the notion that in coronary arterial cells, the activity of ClCa is enhanced by dephosphorylation of the channel or a closely associated regulatory protein. Moreover the balance of CaN and CaMKII regulating ICl(Ca) is dependent on the level of Ca2+ used to activate ICl(Ca).

Indexed as

AnimalsArteriesBenzenesulfonamidesBenzylaminesCalcineurinCalcineurin InhibitorsCalciumCalcium-Calmodulin-Dependent Protein KinasesCalcium-Calmodulin-Dependent Protein Kinase Type 2Chloride ChannelsCoronary VesselsCyclosporineElectric ConductivityEnzyme InhibitorsImmunohistochemistryMuscle, Smooth, VascularBenzenesulfonamidesBenzylaminesCalcineurincalcineurin-AFCalcineurin InhibitorsCalciumCalcium-Calmodulin-Dependent Protein KinasesCalcium-Calmodulin-Dependent Protein Kinase Type 2Chloride ChannelsCyclosporineEnzyme InhibitorsKN 93Peptide FragmentsSulfonamides

Identifiers

PMID12937294
PMCPMC2343461
OpenAlexW2139976750

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.