scholarly journals Fibroblast Growth Factor 2 Augments Transforming Growth Factor Beta 1 in Inducing Epithelial-Mesenchymal Transition in Human Lung Epithelial Cells

2020 ◽  
Author(s):  
Lamis M.F. El-Baz ◽  
Nahla M. Shoukry ◽  
Mohamed L. Salem ◽  
Hani S. Hafez ◽  
Robert D. Guzy
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Human Lung ◽  
Epithelial Mesenchymal Transition ◽  
Lung Epithelial Cells ◽  
Mesenchymal Transition ◽  
Lung Epithelial ◽  
Growth Factor Beta ◽  
Journal Submission

Abstract The authors have withdrawn the journal submission associated with this preprint and requested that the preprint also be withdrawn.

scholarly journals Fibroblast Growth Factor 2 Augments Transforming Growth Factor Beta 1 in Inducing Epithelial-Mesenchymal Transition in Human Lung Epithelial Cells

2019 ◽  
Author(s):  
Lamis M.F. El-Baz ◽  
Nahla M. Shoukry ◽  
Mohamed L. Salem ◽  
Hani S. Hafez ◽  
Robert D. Guzy
Keyword(s):  
Wound Healing ◽  
Growth Factor ◽  
Epithelial Cells ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Human Lung ◽  
A549 Cells ◽  
Lung Epithelial Cells ◽  
Mesenchymal Transition ◽  
Lung Epithelial

Abstract Background: Epithelial-mesenchymal transition (EMT) is a critical event in wound healing and tissue repair following injury. Transforming growth factor beta-1 (TGFβ1) plays an important role in inducing EMT in lung epithelial cells in vitro and in vivo. As fibroblast growth factor-2 (FGF2) reverses TGFβ1-induced collagen I (COL1A1) and α-smooth muscle actin (Actin alpha 2; ACTA2) expression in primary mouse and human lung fibroblasts, we set out this study to determine the effect of FGF2 on TGFβ1-induced EMT in human lung epithelial cells. Methods: BEAS-2B and A549 cells were treated with recombinant FGF2 (2 nM) with or without TGFβ1 (2 ng/ml) for up to 4 days. The phenotypic alterations associated with EMT were assessed by quantitative real-time PCR and E-cadherin protein expression levels was assayed by western blot and immunofluorescence staining. Cell migration was confirmed using wound-healing assay. Results: TGFβ1 treatment led to significantly reduced expression of E-cadherin (CDH1) and markedly induced expression of mesenchymal proteins such as N-cadherin (CDH2), tenascin C (TNC), fibronectin (FN), ACTA2 and COL1A1. TGFβ1 also induced a morphological change and a significant increase in cell migration. FGF2 did not significantly alter EMT gene expression markers on its own, however enhanced TGFβ1-induced suppression of CDH1 and upregulation of ACTA2, but did not alter TNC, FN and CDH2 gene expression levels induced by TGFβ1. FGF2 maintained TGFβ1-induced morphologic changes as well as increased the migration of TGFβ1-treated cells. Furthermore, FGF2 treatment significantly inhibited TGFβ1-induced COL1A1 expression in both BEAS-2B and A549 cells. FGFR-specific tyrosine kinase inhibitor PD173074 blocked the synergism between these two growth factors. Conclusions: This study suggests a synergistic effect between TGFβ1 and FGF2 in inducing EMT, which may play an important role in wound healing and tissue repair after injury. Our findings provide insight into the effects of FGF2 following lung injury and in pulmonary fibrosis.

Abstract A03: Effectiveness of melatonin on the epithelial mesenchymal transition after induction with transforming growth factor beta (TGF-β)

2015 ◽  
Author(s):  
Naiane do Nascimento Gonçalves ◽  
Lívia Carvalho Ferreira ◽  
Juliana Ramos Lopes ◽  
Larissa Bazela Maschio ◽  
Marina Gobbe Moschetta ◽  
...  
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Epithelial Mesenchymal Transition ◽  
Mesenchymal Transition ◽  
Growth Factor Beta
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