Evidence map›Paper›PMID 8618921›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1995

Pulmonary malformation in transgenic mice expressing human keratinocyte growth factor in the lung.

W S Simonet, M L DeRose, N Bucay, H Q Nguyen, S E Wert, L Zhou, T R Ulich, A Thomason, D M Danilenko, J A Whitsett

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
13.8field-weighted citation impact, top 1% 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

30 citing papers in PubMed, 183 citations in OpenAlex.

  1. Article
  2. Congenital lung malformations.Nature reviews. Disease primers · 2023
    Review
  3. Article
  4. Mechanics of Lung Development.Advances in anatomy, embryology, and cell biology · 2023
    Article
  5. Defining the spatial landscape of KRAS mutated congenital pulmonary airway malformations: a distinct entity with a spectrum of histopathologic features.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2022
    Article
  6. Review
  7. Article
  8. Organ-Specific Branching Morphogenesis.Frontiers in cell and developmental biology · 2021
    Review
  9. FGF/FGFR signaling in health and disease.Signal transduction and targeted therapy · 2020
    Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Epithelial repair mechanisms in the lung.American journal of physiology. Lung cellular and molecular physiology · 2010
    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

10 authors at 1 institution in 1 country.

W S SimonetDepartment of Developmental Biology, Amgen, Amgen Center, Thousand Oaks, CA 91320-1789, USA.
M L DeRose
N Bucay
H Q Nguyen
S E Wert
L Zhou
T R Ulich
A Thomason
D M Danilenko
J A Whitsett
Amgen (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Expression of human keratinocyte growth factor (KGF/FGF-7) was directed to epithelial cells of the developing embryonic lung of transgenic mice disrupting normal pulmonary morphogenesis during the pseudoglandular stage of development. By embryonic day 15.5(E15.5), lungs of transgenic surfactant protein C (SP-C)-KGF mice resembled those of humans with pulmonary cystadenoma. Lungs were cystic, filling the thoracic cavity, and were composed of numerous dilated saccules lined with glycogen-containing columnar epithelial cells. The normal distribution of SP-C proprotein in the distal regions of respiratory tubules was disrupted. Columnar epithelial cells lining the papillary structures stained variably and weakly for this distal respiratory cell marker. Mesenchymal components were preserved in the transgenic mouse lungs, yet the architectural relationship of the epithelium to the mesenchyme was altered. SP-C-KGF transgenic mice failed to survive gestation to term, dying before E17.5. Culturing mouse fetal lung explants in the presence of recombinant human KGF also disrupted branching morphogenesis and resulted in similar cystic malformation of the lung. Thus, it appears that precise temporal and spatial expression of KGF is likely to play a crucial role in the control of branching morphogenesis during fetal lung development.

Indexed as

Fibroblast Growth FactorsAnimalsBiomarkersCystadenomaEmbryonic and Fetal DevelopmentFetal DeathFibroblast Growth Factor 10Fibroblast Growth Factor 7Gestational AgeGrowth SubstancesHumansLungLung NeoplasmsMiceMice, TransgenicPromoter Regions, GeneticBiomarkersFGF7 protein, humanFgf7 protein, mouseFibroblast Growth Factor 10Fibroblast Growth Factor 7Fibroblast Growth FactorsGrowth SubstancesProteolipidsPulmonary SurfactantsRNA, Messenger

Identifiers

PMID8618921
PMCPMC40377
OpenAlexW2125921102

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.