Evidence map›Paper›PMID 19785652›Full record

ArticleBritish journal of pharmacology2009

Regulation by FK506 and rapamycin of Ca2+ release from the sarcoplasmic reticulum in vascular smooth muscle: the role of FK506 binding proteins and mTOR.

D MacMillan, J G McCarron

Open access · bronzeAbstract read
In one paragraph

Article in British journal of pharmacology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.1field-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

24 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
  2. Article
  3. FK506 impairs neutrophil migration that results in increased polymicrobial sepsis susceptibility.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023
    Article
  4. Article
  5. FK506 regulates CaBritish journal of pharmacology · 2020
    Article
  6. Skeletal muscle mTORC1 regulates neuromuscular junction stability.Journal of cachexia, sarcopenia and muscle · 2020
    Article
  7. Article
  8. Article
  9. Review
  10. FK506-Binding Protein 12.6/1b, a Negative Regulator of [CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2018
    Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. mTOR and vascular remodeling in lung diseases: current challenges and therapeutic prospects.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2013
    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

2 authors at 1 institution in 1 country.

D MacMillanStrathclyde Institute of Pharmacy and Biomedical Sciences, University of Strathclyde, Glasgow, UK.
J G McCarron
University of Strathclyde · GB

Funding

British Heart Foundation PG/08/066Wellcome Trust 078054/2/05/Z
6 · The paper itself

Abstract

background and purposeThe sarcoplasmic reticulum (SR), regulates the cytoplasmic Ca(2+) concentration ([Ca(2+)](cyto)) in vascular smooth muscle. Release from the SR is controlled by two intracellular receptor/channel complexes, the ryanodine receptor (RyR) and the inositol 1,4,5-trisphosphate receptor (IP(3)R). These receptors may be regulated by the accessory FK506-binding protein (FKBP) either directly, by binding to the channel, or indirectly via FKBP modulation of two targets, the phosphatase, calcineurin or the kinase, mammalian target of rapamycin (mTOR). EXPERIMENTAL APPROACH: Single portal vein myocytes were voltage-clamped in whole cell configuration and [Ca(2+)](cyto) measured using fluo-3. IP(3)Rs were activated by photolysis of caged IP(3) and RyRs activated by hydrostatic application of caffeine. KEY

resultsFK506 which displaces FKBP from each receptor (to inhibit calcineurin) increased the [Ca(2+)](cyto) rise evoked by activation of either RyR or IP(3)R. Rapamycin which displaces FKBP (to inhibit mTOR) also increased the amplitude of the caffeine-evoked, but reduced the IP(3)-evoked [Ca(2+)](cyto) rise. None of the phosphatase inhibitors, cypermethrin, okadaic acid or calcineurin inhibitory peptide, altered either caffeine- or IP(3)-evoked [Ca(2+)](cyto) release; calcineurin did not contribute to FK506-mediated potentiation of RyR- or IP(3)R-mediated Ca(2+) release. The mTOR inhibitor LY294002, like rapamycin, decreased IP(3)-evoked Ca(2+) release. CONCLUSIONS AND IMPLICATIONS: Ca(2+) release in portal vein myocytes, via RyR, was modulated directly by FKBP binding to the channel; neither calcineurin nor mTOR contributed to this regulation. However, IP(3)R-mediated Ca(2+) release, while also modulated directly by FKBP may be additionally regulated by mTOR. Rapamycin inhibition of IP(3)-mediated Ca(2+) release may be explained by mTOR inhibition.

Indexed as

Aniline CompoundsAnimalsCalciumElectrophysiologyFluorescent DyesGuinea PigsImmunosuppressive AgentsMaleMuscle, Smooth, VascularPatch-Clamp TechniquesPortal VeinSarcoplasmic ReticulumSirolimusTacrolimusTacrolimus Binding ProteinsXanthenesAniline CompoundsCalciumFluo-3Fluorescent DyesImmunosuppressive AgentsSirolimusTacrolimusTacrolimus Binding ProteinsXanthenes

Identifiers

PMID19785652
PMCPMC2785532
OpenAlexW1484397562

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.