Evidence map›Paper›PMID 26115671›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2015

Junctional abnormalities in human airway epithelial cells expressing F508del CFTR.

Samuel A Molina, Brandon Stauffer, Hannah K Moriarty, Agnes H Kim, Nael A McCarty, Michael Koval

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Lung cellular and molecular physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
5.0field-weighted citation impact, top 4% 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

37 citing papers in PubMed, 55 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. CFTR as a therapeutic target for severe lung infection.American journal of physiology. Lung cellular and molecular physiology · 2025
    Review
  5. Article
  6. Article
  7. Chronic hyperglycemia aggravates lung function in aAmerican journal of physiology. Lung cellular and molecular physiology · 2024
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. CFTR, Cell Junctions and the Cytoskeleton.International journal of molecular sciences · 2022
    Review
  14. Article
  15. Mucosal Immunity in Cystic Fibrosis.Journal of immunology (Baltimore, Md. : 1950) · 2021
    Review
  16. Pathophysiology of Lung Disease and Wound Repair in Cystic Fibrosis.Pathophysiology : the official journal of the International Society for Pathophysiology · 2021
    Review
  17. Review
  18. Article
  19. Review
  20. Modifying and IntegratingFrontiers in bioengineering and biotechnology · 2020
    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

6 authors at 1 institution in 1 country.

Samuel A MolinaEmory+Children's Center for Cystic Fibrosis and Airways Disease Research, Emory University School of Medicine and Children's Healthcare of Atlanta, Atlanta, Georgia; Division of Pulmonary, Allergy, Critical Care, and Sleep Medicine, Department of Medicine, Emory University School of Medicine, Atlanta, Georgia; Department of Cell Biology, Emory University School of Medicine, Atlanta, Georgia; and s.a.molina@emory.edu.ORCID http://orcid.org/0000-0002-5861-3390
Brandon StaufferEmory+Children's Center for Cystic Fibrosis and Airways Disease Research, Emory University School of Medicine and Children's Healthcare of Atlanta, Atlanta, Georgia; Division of Pulmonary, Allergy/Immunology, Cystic Fibrosis, and Sleep, Department of Pediatrics, Emory University School of Medicine and Children's Healthcare of Atlanta, Atlanta, Georgia.
Hannah K MoriartyDivision of Pulmonary, Allergy, Critical Care, and Sleep Medicine, Department of Medicine, Emory University School of Medicine, Atlanta, Georgia;
Agnes H KimDivision of Pulmonary, Allergy, Critical Care, and Sleep Medicine, Department of Medicine, Emory University School of Medicine, Atlanta, Georgia;
Nael A McCartyEmory+Children's Center for Cystic Fibrosis and Airways Disease Research, Emory University School of Medicine and Children's Healthcare of Atlanta, Atlanta, Georgia; Division of Pulmonary, Allergy/Immunology, Cystic Fibrosis, and Sleep, Department of Pediatrics, Emory University School of Medicine and Children's Healthcare of Atlanta, Atlanta, Georgia.
Michael KovalEmory+Children's Center for Cystic Fibrosis and Airways Disease Research, Emory University School of Medicine and Children's Healthcare of Atlanta, Atlanta, Georgia; Division of Pulmonary, Allergy, Critical Care, and Sleep Medicine, Department of Medicine, Emory University School of Medicine, Atlanta, Georgia; Department of Cell Biology, Emory University School of Medicine, Atlanta, Georgia; and.ORCID http://orcid.org/0000-0002-5422-5614
Emory University · US

Funding

Institutional Training Grant in Alcohol ResearchT32AA013528 · NIAAA · EMORY UNIVERSITY · PI GUIDOT, DAVID MARSHALL · 2002 to 2011
$3.2M
Molecular regulation of pulmonary tight junctionsR01HL116958 · NHLBI · EMORY UNIVERSITY · PI KOVAL, MICHAEL H. · 2013 to 2016
$1.5M
NHLBI NIH HHS R01 HL116958NHLBI NIH HHS R01-HL-116958NIAAA NIH HHS T32 AA013528NIAAA NIH HHS T32-AA-013528
6 · The paper itself

Abstract

Cystic fibrosis (CF) has a profound impact on airway physiology. Accumulating evidence suggests that intercellular junctions are impaired in CF. We examined changes to CF transmembrane conductance regulator (CFTR) function, tight junctions, and gap junctions in NuLi-1 (CFTR(wt/wt)) and CuFi-5 (CFTR(ΔF508/ΔF508)) cells. Cells were studied at air-liquid interface (ALI) and compared with primary human bronchial epithelial cells. On the basis of fluorescent lectin binding, the phenotype of the NuLi-1 and CuFi-5 cells at week 8 resembled that of serous, glycoprotein-rich airway cells. After week 7, CuFi-5 cells possessed 130% of the epithelial Na(+) channel activity and 17% of the CFTR activity of NuLi-1 cells. In both cell types, expression levels of CFTR were comparable to those in primary airway epithelia. Transepithelial resistance of NuLi-1 and CuFi-5 cells stabilized during maturation in ALI culture, with significantly lower transepithelial resistance for CuFi-5 than NuLi-1 cells. We also found that F508del CFTR negatively affects gap junction function in the airway. NuLi-1 and CuFi-5 cells express the connexins Cx43 and Cx26. While both connexins were properly trafficked by NuLi-1 cells, Cx43 was mistrafficked by CuFi-5 cells. Cx43 trafficking was rescued in CuFi-5 cells treated with 4-phenylbutyric acid (4-PBA), as assessed by intracellular dye transfer. 4-PBA-treated CuFi-5 cells also exhibited an increase in forskolin-induced CFTR-mediated currents. The Cx43 trafficking defect was confirmed using IB3-1 cells and found to be corrected by 4-PBA treatment. These data support the use of NuLi-1 and CuFi-5 cells to examine the effects of F508del CFTR expression on tight junction and gap junction function in the context of serous human airway cells.

Indexed as

AdultCalcium SignalingCell LineColforsinConnexin 26Connexin 43ConnexinsCystic FibrosisCystic Fibrosis Transmembrane Conductance RegulatorEpithelial CellsGap JunctionsHumansMalePhenylbutyratesProtein TransportRespiratory Mucosa4-phenylbutyric acidCFTR protein, humanColforsinConnexin 26Connexin 43ConnexinsCystic Fibrosis Transmembrane Conductance RegulatorGJB2 protein, humanPhenylbutyratesair-liquid culturecell modelconnexincystic fibrosisdifferentiationgap junctionnormal lung

Identifiers

PMID26115671
PMCPMC4556929
OpenAlexW1924041829

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.