Evidence map›Paper›PMID 18845610›Full record

ArticleThe Journal of physiology2008

Altered expression of triadin 95 causes parallel changes in localized Ca2+ release events and global Ca2+ signals in skeletal muscle cells in culture.

János Fodor, Monika Gönczi, Monika Sztretye, Beatrix Dienes, Tamás Oláh, László Szabó, Eszter Csoma, Péter Szentesi, Gyula P Szigeti, Isabelle Marty and 1 more

Open access · greenAbstract read
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 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.4field-weighted citation impact, top 21% 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

22 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
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  3. Impaired Intracellular CaInternational journal of molecular sciences · 2022
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  15. Trisk 32 regulates IP(3) receptors in rat skeletal myoblasts.Pflugers Archiv : European journal of physiology · 2011
    Article
  16. On the footsteps of Triadin and its role in skeletal muscle.World journal of biological chemistry · 2011
    Article
  17. Article
  18. Article
  19. Triadin deletion induces impaired skeletal muscle function.The Journal of biological chemistry · 2009
    Article
  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

11 authors at 2 institutions in 3 countries.

János FodorDepartment of Physiology, University of Debrecen, P.O. Box 22, Hungary. csl@phys.dote.hu
Monika Gönczi
Monika Sztretye
Beatrix Dienes
Tamás Oláh
László Szabó
Eszter Csoma
Péter Szentesi
Gyula P Szigeti
Isabelle Marty
László Csernoch
University of Debrecen · HUGrenoble Institute of Neurosciences · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The 95 kDa triadin (Trisk 95), an integral protein of the sarcoplasmic reticular membrane in skeletal muscle, interacts with both the ryanodine receptor (RyR) and calsequestrin. While its role in the regulation of calcium homeostasis has been extensively studied, data are not available on whether the overexpression or the interference with the expression of Trisk 95 would affect calcium sparks the localized events of calcium release (LCRE). In the present study LCRE and calcium transients were studied using laser scanning confocal microscopy on C2C12 cells and on primary cultures of skeletal muscle. Liposome- or adenovirus-mediated Trisk 95 overexpression and shRNA interference with triadin translation were used to modify the level of the protein. Stable overexpression in C2C12 cells significantly decreased the amplitude and frequency of calcium sparks, and the frequency of embers. In line with these observations, depolarization-evoked calcium transients were also suppressed. Similarly, adenoviral transfection of Trisk 95 into cultured mouse skeletal muscle cells significantly decreased both the frequency and amplitude of spontaneous global calcium transients. Inhibition of endogenous triadin expression by RNA interference caused opposite effects. Primary cultures of rat skeletal muscle cells expressing endogenous Trisk 95 readily generated spontaneous calcium transients but rarely produced calcium sparks. Their transfection with specific shRNA sequence significantly reduced the triadin-specific immunoreactivity. Functional experiments on these cells revealed that while caffeine-evoked calcium transients were reduced, LCRE appeared with higher frequency. These results suggest that Trisk 95 negatively regulates RyR function by suppressing localized calcium release events and global calcium signals in cultured muscle cells.

Indexed as

AnimalsCaffeineCalciumCalcium SignalingCarrier ProteinsCell LineCells, CulturedElectric StimulationIntracellular Signaling Peptides and ProteinsMiceMice, Inbred StrainsMicroscopy, ConfocalMuscle Fibers, SkeletalMuscle ProteinsPotassium ChlorideRatsCaffeineCalciumCarrier ProteinsIntracellular Signaling Peptides and ProteinsMuscle ProteinsPotassium ChlorideTrdn protein, mouseTrdn protein, rat

Identifiers

PMID18845610
PMCPMC2655396
OpenAlexW1602557480

What OpenQuestion holds

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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.