Evidence map›Paper›PMID 33463102›Full record

ArticleIranian journal of allergy, asthma, and immunology2020

Fibroblast Growth Factor 2 Augments Transforming Growth Factor Beta 1 Induced Epithelial-mesenchymal Transition in Lung Cell Culture Model.

Lamis M F El-Baz, Nahla M Shoukry, Hani S Hafez, Robert D Guzy, Mohamed Labib Salem

Open access · goldAbstract read
In one paragraph

Article in Iranian journal of allergy, asthma, and immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.9field-weighted citation impact, top 22% 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

5 citing papers in PubMed, 10 citations in OpenAlex.

  1. Review
  2. Review
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  5. 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

5 authors at 3 institutions in 2 countries.

Lamis M F El-BazDepartment of Medicine, Section of Pulmonary and Critical Care Medicine, University of Chicago, Chicago, Illinois, USA AND Department of Zoology, Faculty of Science, Suez University, Suez, Egypt. lamis.albaz@suezuniv.edu.eg.
Nahla M ShoukryDepartment of Zoology, Faculty of Science, Suez University, Suez, Egypt. nahla.shokry@suezuniv.edu.eg.
Hani S HafezDepartment of Zoology, Faculty of Science, Suez University, Suez, Egypt. hani.hafez@suezuniv.edu.eg.
Robert D GuzyDepartment of Medicine, Section of Pulmonary and Critical Care Medicine, University of Chicago, Chicago, Illinois, USA. rguzy1@bsd.uchicago.edu.
Mohamed Labib SalemDepartment of Immunology and Biotechnology, Faculty of Science, Center of Excellence in Cancer Research, Tanta University, Tanta, Egypt. mohamedlabibsalem@yahoo.com.
Suez University · EGTanta University · EGUniversity of Chicago · US

Funding

Mechanism of Fibroblast Growth Factor 2-Mediated Alveolar Epithelial RepairK08HL125910 · NHLBI · UNIVERSITY OF CHICAGO · PI GUZY, ROBERT DAVID · 2017 to 2021
$820k
NHLBI NIH HHS K08 HL125910
6 · The paper itself

Abstract

Impaired lung epithelial cell regeneration following injury may contribute to the development of pulmonary fibrosis. Epithelial-mesenchymal transition (EMT) is a critical event in embryonic development, wound healing following injury, and even cancer progression. Previous studies have shown that the combination of transforming growth factor beta-1 (TGFβ1) and fibroblast growth factor 2 (FGF2) induces EMT during cancer metastasis. However, this synergy remains to be elucidated in inducing EMT associated with wound healing after injury. We set out this study to determine the effect of fibroblast growth factor 2 (FGF2) on TGFβ1-induced EMT in the human lung epithelium. BEAS-2B and A549 cells were treated with TGFβ1, FGF2, or both. EMT phenotype was investigated morphologically and by measuring mRNA expression levels; using quantitative real-time PCR. E-cadherin expression was assayed by western blot and immunofluorescence staining. Cell migration was confirmed using a wound-healing assay. TGFβ1 induced a morphological change and a significant increase in cell migration of BEAS-2B cells. TGFβ1 significantly reduced E-cadherin (CDH1) mRNA expression and markedly induced expression of N-cadherin (CDH2), tenascin C (TNC), fibronectin (FN), actin alpha 2 (ACTA2), and collagen I (COL1A1). While FGF2 alone did not significantly alter EMT gene expression, it enhanced TGFβ1-induced suppression of CDH1 and upregulation of ACTA2, but not TNC, FN, and CDH2. FGF2 significantly inhibited TGFβ1-induced COL1A1 expression. Furthermore, FGF2 maintained TGFβ1-induced morphologic changes and increased the migration of TGFβ1-treated cells. This study suggests a synergistic effect between TGFβ1 and FGF2 in inducing EMT in lung epithelial cells, which may play an important role in wound healing and tissue repair after injury.

Indexed as

Epithelial-Mesenchymal TransitionBiomarkersCell Culture TechniquesCell Line, TumorCells, CulturedEpithelial CellsFibroblast Growth Factor 2Gene Expression RegulationHumansProtein Kinase InhibitorsTransforming Growth Factor beta1BiomarkersFibroblast Growth Factor 2Protein Kinase InhibitorsTransforming Growth Factor beta1Epithelial cellsEpithelial-mesenchymal transitionFibroblast growth factor 2Lung injuryTransforming growth factor beta1

Identifiers

PMID33463102
PMCPMC8366022
OpenAlexW3083464928

What OpenQuestion holds

Textmetadata
LicenceTDM
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.