Evidence map›Paper›PMID 22183723›Full record

ArticleThe Journal of physiology2012

A self-limiting regulation of vasoconstrictor-activated TRPC3/C6/C7 channels coupled to PI(4,5)P₂-diacylglycerol signalling.

Yuko Imai, Kyohei Itsuki, Yasushi Okamura, Ryuji Inoue, Masayuki X Mori

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
1.9field-weighted citation impact, top 18% 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

41 citing papers in PubMed, 57 citations in OpenAlex.

  1. Review
  2. The role of IPPflugers Archiv : European journal of physiology · 2026
    Review
  3. CaNeurochemical research · 2026
    Article
  4. Review
  5. Review
  6. PIPNature communications · 2024
    Article
  7. Article
  8. Article
  9. Article
  10. TRPC6, a therapeutic target for pulmonary hypertension.American journal of physiology. Lung cellular and molecular physiology · 2021
    Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. TRPC4 as a coincident detector of GCurrent opinion in physiology · 2020
    Article
  16. Obligatory role for PKCδ in PIPThe Journal of physiology · 2020
    Article
  17. Review
  18. Engineering an enhanced voltage-sensing phosphatase.The Journal of general physiology · 2020
    Article
  19. Review
  20. 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

5 authors at 2 institutions in 1 country.

Yuko ImaiDepartment of Physiology, School of Medicine, Fukuoka University, Fukuoka 814-0180, Japan.
Kyohei Itsuki
Yasushi Okamura
Ryuji Inoue
Masayuki X Mori
Fukuoka University · JPOsaka University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Activation of transient receptor potential (TRP) canonical TRPC3/C6/C7 channels by diacylglycerol (DAG) upon stimulation of phospholipase C (PLC)-coupled receptors results in the breakdown of phosphoinositides (PIPs). The critical importance of PIPs to various ion-transporting molecules is well documented, but their function in relation to TRPC3/C6/C7 channels remains controversial. By using an ectopic voltage-sensing PIP phosphatase (DrVSP), we found that dephosphorylation of PIPs robustly inhibits currents induced by carbachol (CCh), 1-oleolyl-2-acetyl-sn-glycerol (OAG) or RHC80267 in TRPC3, TRPC6 and TRPC7 channels, though the strength of the DrVSP-mediated inhibition (VMI) varied among the channels with a rank order of C7>C6>C3. Pharmacological and molecular interventions suggest that depletion of phosphatidylinositol 4,5-bisphosphate (PI(4,5)P₂) is most likely the critical event for VMI in all three channels.When the PLC catalytic signal was vigorously activated through overexpression of the muscarinic type-I receptor (M1R), the inactivation of macroscopic TRPC currents was greatly accelerated in the same rank order as the VMI, and VMI of these currents was attenuated or lost. VMI was also rarely detected in vasopressin-induced TRPC6-like currents inA7r5 vascular smooth muscle cells, indicating that the inactivation by PI(4,5)P₂ depletion underlies the physiological condition. Simultaneous fluorescence resonance energy transfer (FRET)-based measurement of PI(4,5)P₂ levels and TRPC6 currents confirmed that VMI magnitude reflects the degree of PI(4,5)P₂ depletion. These results demonstrate that TRPC3/C6/C7 channels are differentially regulated by depletion of PI(4,5)P₂, and that the bimodal signal produced by PLC activation controls these channels in a self-limiting manner.

Indexed as

AnimalsArginine VasopressinDiglyceridesHEK293 CellsHumansPhosphatidylinositol 4,5-DiphosphateReceptor, Muscarinic M1TRPC Cation ChannelsType C PhospholipasesVasoconstrictor AgentsZebrafish1,2-diacylglycerolArginine VasopressinDiglyceridesPhosphatidylinositol 4,5-DiphosphateReceptor, Muscarinic M1TRPC3 cation channelTRPC Cation ChannelsType C PhospholipasesVasoconstrictor Agents

Identifiers

PMID22183723
PMCPMC3381819
OpenAlexW1552720600

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.