Evidence map›Paper›PMID 18458941›Full record

ArticlePflugers Archiv : European journal of physiology2008

Functional coupling of TRPV4 cationic channel and large conductance, calcium-dependent potassium channel in human bronchial epithelial cell lines.

José M Fernández-Fernández, Yaniré N Andrade, Maite Arniges, Jacqueline Fernandes, Cristina Plata, Francisca Rubio-Moscardo, Esther Vázquez, Miguel A Valverde

Abstract read
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In one paragraph

Article in Pflugers Archiv : European journal of physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
1.3field-weighted citation impact, top 24% 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

32 citing papers in PubMed, 1 synthesis or guideline pooled it, 71 citations in OpenAlex.

  1. Pooled it
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  16. Article
  17. Fluid-induced lung injury-role of TRPV4 channels.Pflugers Archiv : European journal of physiology · 2017
    Article
  18. TRP functions in the broncho-pulmonary system.Seminars in immunopathology · 2016
    Review
  19. How does rhinovirus cause the common cold cough?BMJ open respiratory research · 2016
    Article
  20. Genetic deficit of KBritish journal of pharmacology · 2015
    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

8 authors at 1 institution in 1 country.

José M Fernández-FernándezDepartment of Experimental and Health Sciences, Universitat Pompeu Fabra, PRBB, C/ Dr. Aiguader 88, Barcelona, 08003, Spain.
Yaniré N Andrade
Maite Arniges
Jacqueline Fernandes
Cristina Plata
Francisca Rubio-Moscardo
Esther Vázquez
Miguel A Valverde
Pompeu Fabra University · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Calcium-dependent potassium channels are implicated in electrolyte transport, cell volume regulation and mechanical responses in epithelia, although the pathways for calcium entry and their coupling to the activation of potassium channels are not fully understood. We now show molecular evidence for the presence of TRPV4, a calcium permeable channel sensitive to osmotic and mechanical stress, and its functional coupling to the large conductance calcium-dependent potassium channel (BK(Ca)) in a human bronchial epithelial cell line (HBE). Reverse transcriptase polymerase chain reaction, intracellular calcium imaging and whole-cell patch-clamp experiments using HBE cells demonstrated the presence of TRPV4 messenger and Ca(2+) entry, and outwardly rectifying cationic currents elicited by the TRPV4 specific activator 4alpha-phorbol 12,13-didecanoate (4alphaPDD). Cell-attached and whole-cell patch-clamp of HBE cells exposed to 4alphaPDD, and hypotonic and high-viscosity solutions (related to mechanical stress) revealed the activation of BK(Ca) channels subsequent to extracellular Ca(2+) influx via TRPV4, an effect lost upon antisense-mediated knock-down of TRPV4. Further analysis of BK(Ca) modulation after TRPV4 activation showed that the Ca(2+) signal can be generated away from the BK(Ca) location at the plasma membrane, and it is not mediated by intracellular Ca(2+) release via ryanodine receptors. Finally, we have shown that, unlike the reported disengagement of TRPV4 and BK(Ca) in response to hypotonic solutions, cystic fibrosis bronchial epithelial cells (CFBE) preserve the functional coupling of TRPV4 and BK(Ca) in response to high-viscous solutions.

Indexed as

BronchiCell LineCystic FibrosisElectrophysiologyEpithelial CellsHumansHypotonic SolutionsLarge-Conductance Calcium-Activated Potassium ChannelsOligoribonucleotides, AntisenseOsmotic PressurePhorbol EstersReverse Transcriptase Polymerase Chain ReactionTRPV Cation ChannelsViscosityHypotonic SolutionsLarge-Conductance Calcium-Activated Potassium ChannelsOligoribonucleotides, Antisensephorbol-12,13-didecanoatePhorbol EstersTRPV4 protein, humanTRPV Cation Channels

Identifiers

PMID18458941
OpenAlexW2159738437

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.