Evidence map›Paper›PMID 12198094›Full record

ArticleThe Journal of general physiology2002

Regulation of murine airway surface liquid volume by CFTR and Ca2+-activated Cl- conductances.

Robert Tarran, Matthew E Loewen, Anthony M Paradiso, John C Olsen, Micheal A Gray, Barry E Argent, Richard C Boucher, Sherif E Gabriel

Open access · hybridAbstract readComparative Study
In one paragraph

Article in The Journal of general physiology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

56 citing papers in PubMed, 124 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Lung Microbiome in Cystic Fibrosis.Life (Basel, Switzerland) · 2021
    Review
  5. Review
  6. Article
  7. Article
  8. Concurrent absorption and secretion of airway surface liquids and bicarbonate secretion in human bronchioles.American journal of physiology. Lung cellular and molecular physiology · 2019
    Article
  9. Article
  10. Article
  11. CaNature communications · 2019
    Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Role of CFTR in epithelial physiology.Cellular and molecular life sciences : CMLS · 2017
    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

8 authors at 1 institution in 1 country.

Robert TarranCystic Fibsosis/Pulmonary Research and Treatment Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA. tarran@uclink.berkeley.edu
Matthew E Loewen
Anthony M Paradiso
John C Olsen
Micheal A Gray
Barry E Argent
Richard C Boucher
Sherif E Gabriel
University of North Carolina at Chapel Hill · US

Funding

IDENTIFICATION OF CA2+ REGULATED APICAL CL- CHANNELSR01HL062564 · NHLBI · UNIVERSITY OF NORTH CAROLINA CHAPEL HILL · PI GABRIEL, SHERIF E · 2000 to 2003
$867k
NHLBI NIH HHS HL62564NHLBI NIH HHS R01 HL062564
6 · The paper itself

Abstract

Two Cl(-) conductances have been described in the apical membrane of both human and murine proximal airway epithelia that are thought to play predominant roles in airway hydration: (1) CFTR, which is cAMP regulated and (2) the Ca(2+)-activated Cl(-) conductance (CaCC) whose molecular identity is uncertain. In addition to second messenger regulation, cross talk between these two channels may also exist and, whereas CFTR is absent or defective in cystic fibrosis (CF) airways, CaCC is preserved, and may even be up-regulated. Increased CaCC activity in CF airways is controversial. Hence, we have investigated the effects of CFTR on CaCC activity and have also assessed the relative contributions of these two conductances to airway surface liquid (ASL) height (volume) in murine tracheal epithelia. We find that CaCC is up-regulated in intact murine CF tracheal epithelia, which leads to an increase in UTP-mediated Cl(-)/volume secretion. This up-regulation is dependent on cell polarity and is lost in nonpolarized epithelia. We find no role for an increased electrical driving force in CaCC up-regulation but do find an increased Ca(2+) signal in response to mucosal nucleotides that may contribute to the increased Cl(-)/volume secretion seen in intact epithelia. CFTR plays a critical role in maintaining ASL height under basal conditions and accordingly, ASL height is reduced in CF epithelia. In contrast, CaCC does not appear to significantly affect basal ASL height, but does appear to be important in regulating ASL height in response to released agonists (e.g., mucosal nucleotides). We conclude that both CaCC and the Ca(2+) signal are increased in CF airway epithelia, and that they contribute to acute but not basal regulation of ASL height.

Indexed as

AnimalsCalciumCell LineChloride ChannelsCystic Fibrosis Transmembrane Conductance RegulatorIn Vitro TechniquesMembrane PotentialsMiceMice, Inbred BALB CMice, Inbred C57BLMice, TransgenicRespiratory MucosaCalciumChloride ChannelsCystic Fibrosis Transmembrane Conductance Regulator

Identifiers

PMID12198094
PMCPMC2229523
OpenAlexW2109053981

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.