Evidence map›Paper›PMID 21690189›Full record

ArticleThe Journal of physiology2011

Regulation of bradykinin-induced activation of volume-sensitive outwardly rectifying anion channels by Ca2+ nanodomains in mouse astrocytes.

Tenpei Akita, Yasunobu Okada

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in The Journal of physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
1.7field-weighted citation impact, top 19% 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

40 citing papers in PubMed, 58 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. NMDARs, Coincidence Detectors of Astrocytic and Neuronal Activities.International journal of molecular sciences · 2021
    Review
  8. Review
  9. Intracellular ClPflugers Archiv : European journal of physiology · 2020
    Review
  10. Roles of TRP Channels in Neurological Diseases.Oxidative medicine and cellular longevity · 2020
    Review
  11. Review
  12. CaFrontiers in cell and developmental biology · 2020
    Article
  13. Article
  14. Review
  15. ATP Release Channels.International journal of molecular sciences · 2018
    Review
  16. Review
  17. Physiology of Astroglia.Physiological reviews · 2018
    Review
  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

2 authors at 1 institution in 1 country.

Tenpei AkitaDepartment of Cell Physiology, National Institute for Physiological Sciences, National Institutes of Natural Sciences, Okazaki 444-8585, Japan.
Yasunobu Okada
National Institute for Physiological Sciences · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Volume-sensitive outwardly rectifying (VSOR) anion channels play a key role in a variety of essential cell functions including cell volume regulation, cell death induction and intercellular communications. We previously demonstrated that, in cultured mouse cortical astrocytes, VSOR channels are activated in response to an inflammatory mediator, bradykinin, even without an increase in cell volume. Here we report that this VSOR channel activation must be mediated firstly by 'nanodomains' of high [Ca2+]i generated at the sites of both Ca2+ release from intracellular Ca2+ stores and Ca2+ entry at the plasma membrane. Bradykinin elicited a [Ca2+]i rise, initially caused by Ca2+ release and then by Ca2+ entry. Suppression of the [Ca2+]i rise by removal of extracellular Ca2+ and by depletion of Ca2+ stores suppressed the VSOR channel activation in a graded manner. Quantitative RT-PCR and suppression of gene expression with small interfering RNAs indicated that Orai1, TRPC1 and TRPC3 channels are involved in the Ca2+ entry and especially the entry through TRPC1 channels is strongly involved in the bradykinin-induced activation of VSOR channels. Moreover, Ca2+-dependent protein kinases Cα and β were found to mediate the activation after the [Ca2+]i rise through inducing generation of reactive oxygen species. Intracellular application of a slow Ca2+ chelator, EGTA, at 10 mM or a fast chelator, BAPTA, at 1 mM, however, had little effect on the VSOR channel activation. Application of BAPTA at 10 mM suppressed significantly the activation to one-third. These suggest that the VSOR channel activation induced by bradykinin is regulated by Ca2+ in the vicinity of individual Ca2+ release and entry channels, providing a basis for local control of cell volume regulation and intercellular communications.

Indexed as

Cell SizeAnimalsAstrocytesBradykininCalciumCell CommunicationCells, CulturedMiceNanoparticlesProtein Structure, TertiaryTRPC Cation ChannelsTRPM Cation ChannelsBradykininCalciumtransient receptor potential cation channel, subfamily C, member 1TRPC3 cation channelTRPC Cation ChannelsTrpm7 protein, mouseTRPM Cation Channels

Identifiers

PMID21690189
PMCPMC3179992
OpenAlexW1581626040

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.