Evidence map›Paper›PMID 14724753›Full record

ArticleThe Journal of membrane biology2003

Modulation of calcium-dependent chloride secretion by basolateral SK4-like channels in a human bronchial cell line.

K Bernard, S Bogliolo, O Soriani, J Ehrenfeld

Abstract read
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In one paragraph

Article in The Journal of membrane biology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
0.6field-weighted citation impact, top 36% 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

25 citing papers in PubMed, 49 citations in OpenAlex.

  1. Potassium Channels of the Airway Epithelium.Acta physiologica (Oxford, England) · 2026
    Review
  2. Review
  3. KBiomedicines · 2023
    Review
  4. Article
  5. CLCA1 Regulates Airway Mucus Production and Ion Secretion Through TMEM16A.International journal of molecular sciences · 2021
    Article
  6. Article
  7. Ion channels of the lung and their role in disease pathogenesis.American journal of physiology. Lung cellular and molecular physiology · 2017
    Review
  8. Article
  9. Pulmonary epithelial barrier function: some new players and mechanisms.American journal of physiology. Lung cellular and molecular physiology · 2015
    Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Characteristics of Kcnn4 channels in the apical membranes of an intestinal epithelial cell line.American journal of physiology. Gastrointestinal and liver physiology · 2011
    Article
  16. Article
  17. Article
  18. Ion transport by pulmonary epithelia.Journal of biomedicine & biotechnology · 2011
    Review
  19. 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

4 authors at 2 institutions in 1 country.

K BernardLaboratoire de Physiologie des Membranes cellulaires, Université de Nice-Sophia Antipolis, UMR 6078/CNRS, 06230 Villefranche-sur-Mer, France.
S Bogliolo
O Soriani
J Ehrenfeld
Université Côte d'Azur · FRCentre National de la Recherche Scientifique · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The human bronchial cell line16HBE14o- was used as a model of airway epithelial cells to study the Ca(2+)-dependent Cl(-) secretion and the identity of K(Ca) channels involved in the generation of a favorable driving force for Cl(-) exit. After ionomycin application, a calcium-activated short-circuit current ( I(sc)) developed, presenting a transient peak followed by a plateau phase. Both phases were inhibited to different degrees by NFA, glybenclamide and NPPB but DIDS was only effective on the peak phase. (86)Rb effluxes through both apical and basolateral membranes were stimulated by calcium, blocked by charybdotoxin, clotrimazole and TPA. 1-EBIO, a SK-channel opener, stimulated (86)Rb effluxes. Block of basolateral K(Ca) channels resulted in I(sc) inhibition but, while reduced, I(sc) was still observed if mucosal Cl(-) was lowered. Among SK family members, only SK4 and SK1 mRNAs were detected by RT-PCR. KCNQ1 mRNAs were also identified, but involvement of K(cAMP) channels in Cl(-) secretion was unlikely, since cAMP application had no effect on (86)Rb effluxes. Moreover, chromanol 293B or clofilium, specific inhibitors of KCNQ1 channels, had no effect on cAMP-dependent I(sc). In conclusion, two distinct components of Cl(-) secretion were identified by a pharmacological approach after a Cai2+ rise. K(Ca) channels presenting the pharmacology of SK4 channels are present on both apical and basolateral membranes, but it is the basolateral SK4-like channels that play a major role in calcium-dependent chloride secretion in 16HBE14o- cells.

Indexed as

Potassium Channels, Calcium-ActivatedAdaptation, PhysiologicalBronchiCalciumCell LineChlorineDose-Response Relationship, DrugElectric ConductivityHumansIntermediate-Conductance Calcium-Activated Potassium ChannelsIon Channel GatingIonomycinMembrane PotentialsPotassium ChannelsRespiratory MucosaRubidiumCalciumChlorineIntermediate-Conductance Calcium-Activated Potassium ChannelsIonomycinKCNN4 protein, humanPotassium ChannelsPotassium Channels, Calcium-ActivatedRubidium

Identifiers

PMID14724753
OpenAlexW2062793852

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.