Evidence map›Paper›PMID 18356201›Full record

ArticleThe Journal of physiology2008

Diverse properties of store-operated TRPC channels activated by protein kinase C in vascular myocytes.

Sohag N Saleh, Anthony P Albert, C M Peppiatt-Wildman, William A Large

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in The Journal of physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
6.5field-weighted citation impact, top 3% 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

56 citing papers in PubMed, 108 citations in OpenAlex.

  1. Article
  2. Article
  3. Genetic evidence against involvement of TRPC proteins in SOCE, ROCE, and CRAC channel function.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  4. Role for the PIPJournal of cell communication and signaling · 2024
    Review
  5. Article
  6. Article
  7. Article
  8. Obligatory role for PKCδ in PIPThe Journal of physiology · 2020
    Article
  9. Article
  10. Review
  11. Article
  12. Calcium signals that determine vascular resistance.Wiley interdisciplinary reviews. Systems biology and medicine · 2019
    Review
  13. Review
  14. Dual action of the GαScientific reports · 2018
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Regulation of Coronary Blood Flow.Comprehensive Physiology · 2017
    Review
  20. Intracellular calcium increases in vascular smooth muscle cells with progression of chronic kidney disease in a rat model.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2017
    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 1 institution in 1 country.

Sohag N SalehIon Channels and Cell Signalling Research Centre, Division of Basic Medical Sciences, St George's, University of London, Cranmer Terrace, London SW17 0RE, UK.
Anthony P Albert
C M Peppiatt-Wildman
William A Large
St George's, University of London · GB

Funding

Wellcome TrustWellcome Trust 072375
6 · The paper itself

Abstract

In vascular smooth muscle, store-operated channels (SOCs) contribute to many physiological functions including vasoconstriction and cell growth and proliferation. In the present work we compared the properties of SOCs in freshly dispersed myocytes from rabbit coronary and mesenteric arteries and portal vein. Cyclopiazonic acid (CPA)-induced whole-cell SOC currents were sixfold greater at negative membrane potentials and displayed markedly different rectification properties and reversal potentials in coronary compared to mesenteric artery myocytes. Single channel studies showed that endothelin-1, CPA and the cell-permeant Ca(2+) chelator BAPTA-AM activated the same 2.6 pS SOC in coronary artery. In 1.5 mM [Ca(2+)](o) the unitary conductance of SOCs was significantly greater in coronary than in mesenteric artery. Moreover in 0 mM [Ca(2+)](o) the conductance of SOCs in coronary artery was unaltered whereas the conductance of SOCs in mesenteric artery was increased fourfold. In coronary artery SOCs were inhibited by the protein kinase C (PKC) inhibitor chelerythrine and activated by the phorbol ester phorbol 12,13-dibutyrate (PDBu), the diacylglycerol analogue 1-oleoyl-2-acetyl-sn-glycerol (OAG) and a catalytic subunit of PKC. These data infer an important role for PKC in activation of SOCs in coronary artery similar to mesenteric artery and portal vein. Anti-TRPC1 and -TRPC5 antibodies inhibited SOCs in coronary and mesenteric arteries and portal vein but anti-TRPC6 blocked SOCs only in coronary artery and anti-TRPC7 blocked SOCs only in portal vein. Immunoprecipitation showed associations between TRPC1 and TRPC5 in all preparations but between TRPC5 and TRPC6 only in coronary artery and between TRPC5 and TRPC7 only in portal vein. Finally, flufenamic acid increased SOC activity in coronary artery but inhibited SOCs in mesenteric artery and portal vein myocytes. These data provide strong evidence that vascular myocytes express diverse SOC isoforms, which are likely to be composed of different TRPC proteins and have different physiological functions.

Indexed as

AnimalsBenzophenanthridinesMembrane PotentialsMesenteric ArteriesMyocytes, Smooth MuscleProtein Kinase CRabbitsTRPC Cation ChannelsBenzophenanthridineschelerythrineProtein Kinase CTRPC Cation Channels

Identifiers

PMID18356201
PMCPMC2408673
OpenAlexW2099236021

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.