Evidence map›Paper›PMID 20833776›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2010

Keratinocyte growth factor enhances barrier function without altering claudin expression in primary alveolar epithelial cells.

Michael J LaFemina, Deepti Rokkam, Anita Chandrasena, Jue Pan, Anisha Bajaj, Meshell Johnson, James A Frank

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Lung cellular and molecular physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
3.4field-weighted citation impact, top 8% 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

39 citing papers in PubMed, 73 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. [A review on the effect of Claudin-18 on bronchopulmonary dysplasia in preterm infants].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2021
    Review
  9. Review
  10. Review
  11. Article
  12. Bioengineering the Blood-gas Barrier.Comprehensive Physiology · 2020
    Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 1 country.

Michael J LaFeminaUniv. of California, San Francisco, NCIRE/VAMC, 94121, USA.
Deepti Rokkam
Anita Chandrasena
Jue Pan
Anisha Bajaj
Meshell Johnson
James A Frank
University of California, San Francisco · USNorthern California Institute for Research and Education · USSan Francisco VA Medical Center · US

Funding

Regulation of alveolar epithelial barrier function by claudinsR01HL088440 · NHLBI · NORTHERN CALIFORNIA INSTITUTE/RES/EDU · PI FRANK, JAMES A · 2007 to 2011
$2.3M
Regulation of alveolar barrier function by claudinsR56HL088440 · NHLBI · NORTHERN CALIFORNIA INSTITUTE/RES/EDU · PI FRANK, JAMES A · 2013 to 2013
$380k
NHLBI NIH HHS HL-088440NHLBI NIH HHS R01 HL088440NHLBI NIH HHS R56 HL088440
6 · The paper itself

Abstract

Keratinocyte growth factor (KGF) has efficacy in several experimental models of lung injury; however, the mechanisms underlying KGF's protective effect remain incompletely understood. This study was undertaken to determine whether KGF augments barrier function in primary rat alveolar epithelial cells grown in culture, specifically whether KGF alters tight junction function via claudin expression. KGF significantly increased alveolar epithelial barrier function in culture as assessed by transepithelial electrical resistance (TER) and paracellular permeability. Fluorescence-activated cell sorting of freshly isolated type 1 (AT1) and type 2 (AT2) cells followed by quantitative real-time RT-PCR revealed that more than 97% of claudin mRNA transcripts in these cells were for claudins-3, -4, and -18. Using cultured AT2 cells, we then examined the effect of KGF on the protein levels of the claudins with the highest mRNA levels: -3, -4, -5, -7, -12, -15, and -18. KGF did not alter the levels of any of the claudins tested, nor of zona occludens-1 (ZO-1) or occludin. Moreover, localization of claudins-3, -4, -18, and ZO-1 was unchanged. KGF did induce a marked increase in the apical perijunctional F-actin ring. Actin depolymerization with cytochalasin D blocked the KGF-mediated increase in TER without significantly changing TER in control cells. Together, these data support a novel mechanism by which KGF enhances alveolar barrier function, modulation of the actin cytoskeleton. In addition, these data demonstrate the complete claudin expression profile for AT1 and AT2 cells and indicate that claudins-3, -4, and -18 are the primary claudins expressed in these cell types.

Indexed as

AnimalsBlood-Air BarrierCells, CulturedClaudinsCytoskeletonEpithelial CellsFibroblast Growth Factor 7HumansMaleMembrane ProteinsProtein IsoformsPulmonary AlveoliRatsRats, Sprague-DawleyRespiratory MucosaTight JunctionsClaudinsFibroblast Growth Factor 7Membrane ProteinsProtein Isoforms

Identifiers

PMID20833776
PMCPMC3006268
OpenAlexW2121072642

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.