Evidence map›Paper›PMID 20093646›Full record

ArticleAmerican journal of respiratory and critical care medicine2010

Fibroblast growth factor receptors control epithelial-mesenchymal interactions necessary for alveolar elastogenesis.

Sorachai Srisuma, Soumyaroop Bhattacharya, Dawn M Simon, Siva K Solleti, Shivraj Tyagi, Barry Starcher, Thomas J Mariani

Abstract read
In one paragraph

Article in American journal of respiratory and critical care medicine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
4.6field-weighted citation impact, top 5% 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

57 citing papers in PubMed, 83 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. Review
  6. Prenatal FGFR2 Signaling via PI3K/AKT Specifies the PDGFRAAmerican journal of respiratory cell and molecular biology · 2024
    Article
  7. Article
  8. FGF18 promotes human lung branching morphogenesis through regulating mesenchymal progenitor cells.American journal of physiology. Lung cellular and molecular physiology · 2023
    Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. FGF/FGFR signaling in health and disease.Signal transduction and targeted therapy · 2020
    Review
  18. Article
  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

7 authors at 3 institutions in 2 countries.

Sorachai SrisumaDivision of Neonatology and Center for Pediatric Biomedical Research, University of Rochester Medical Center, Rochester, New York 14642, USA.
Soumyaroop Bhattacharya
Dawn M Simon
Siva K Solleti
Shivraj Tyagi
Barry Starcher
Thomas J Mariani
Brigham and Women's Hospital · USThe University of Texas Health Science Center at Tyler · USUniversity of Rochester Medical Center · US

Funding

Functional Genomics of AlveogenesisR01HL071885 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI MARIANI, THOMAS J · 2003 to 2006
$1.4M
NHLBI NIH HHS HL071885
6 · The paper itself

Abstract

rationaleThe mechanisms contributing to alveolar formation are poorly understood. A better understanding of these processes will improve efforts to ameliorate lung disease of the newborn and promote alveolar repair in the adult. Previous studies have identified impaired alveogenesis in mice bearing compound mutations of fibroblast growth factor (FGF) receptors (FGFRs) 3 and 4, indicating that these receptors cooperatively promote postnatal alveolar formation.

objectivesTo determine the molecular and cellular mechanisms of FGF-mediated alveolar formation.

methodsCompound FGFR3/FGFR4-deficient mice were assessed for temporal changes in lung growth, airspace morphometry, and genome-wide expression. Observed gene expression changes were validated using quantitative real-time RT-PCR, tissue biochemistry, histochemistry, and ELISA. Autocrine and paracrine regulatory mechanisms were investigated using isolated lung mesenchymal cells and type II pneumocytes. MEASUREMENTS AND MAIN

resultsQuantitative analysis of airspace ontogeny confirmed a failure of secondary crest elongation in compound mutant mice. Genome-wide expression profiling identified molecular alterations in these mice involving aberrant expression of numerous extracellular matrix molecules. Biochemical and histochemical analysis confirmed changes in elastic fiber gene expression resulted in temporal increases in elastin deposition with the loss of typical spatial restriction. No abnormalities in elastic fiber gene expression were observed in isolated mesenchymal cells, indicating that abnormal elastogenesis in compound mutant mice is not cell autonomous. Increased expression of paracrine factors, including insulin-like growth factor-1, in freshly-isolated type II pneumocytes indicated that these cells contribute to the observed pathology.

conclusionsEpithelial/mesenchymal signaling mechanisms appear to contribute to FGFR-dependent alveolar elastogenesis and proper airspace formation.

Indexed as

Analysis of VarianceAnimalsElastinEnzyme-Linked Immunosorbent AssayEpithelial CellsGene ExpressionGene Expression ProfilingGene Expression Regulation, DevelopmentalLungMesodermMiceMice, Inbred C57BLOligonucleotide Array Sequence AnalysisPulmonary AlveoliReceptors, Fibroblast Growth FactorReverse Transcriptase Polymerase Chain ReactionElastinReceptors, Fibroblast Growth Factor

Identifiers

PMID20093646
PMCPMC2854333
OpenAlexW2150807434

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.