ArticleAmerican journal of physiology. Lung cellular and molecular physiology2017
Focal adhesion kinase signaling determines the fate of lung epithelial cells in response to TGF-β.
Article in American journal of physiology. Lung cellular and molecular physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 27 citations in OpenAlex.
- AI-driven discovery of natural product-derived FAK1 inhibitors for idiopathic pulmonary fibrosis.Molecular diversity · 2026Article
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- Dahuang Zhechong pill alleviates pulmonary fibrosis by inhibiting apoptosis and epithelial-mesenchymal transition of type II alveolar epithelial cellsJournal of traditional and complementary medicine · 2026Article
- TGF-β signaling: critical nexus of fibrogenesis and cancer.Journal of translational medicine · 2024Review
- A TGF-β-responsive enhancer regulates SRC expression and epithelial-mesenchymal transition-associated cell migration.Journal of cell science · 2023Article
- mRNA Levels of Epithelial and Mesenchymal Markers in Lung Epithelial Cell Lines.Reports of biochemistry & molecular biology · 2023Article
- Differential bioactivity of four BMP-family members as function of biomaterial stiffness.Biomaterials · 2022Article
- FAK Inhibition Attenuates Corneal Fibroblast Differentiation In Vitro.Biomolecules · 2021Article
- Suppression of TGF-β1 signaling by Matrigel via FAK signaling in cultured human trabecular meshwork cells.Scientific reports · 2021Article
- Mefunidone Ameliorates Bleomycin-Induced Pulmonary Fibrosis in Mice.Frontiers in pharmacology · 2021Article
- Liver epithelial focal adhesion kinase modulates fibrogenesis and hedgehog signaling.JCI insight · 2020Article
- FOXF2 deficiency accelerates the visceral metastasis of basal-like breast cancer by unrestrictedly increasing TGF-β and miR-182-5p.Cell death and differentiation · 2020Article
- Enhancement of FAK alleviates ventilator-induced alveolar epithelial cell injury.Scientific reports · 2020Article
- MiR-92a regulates endothelial progenitor cells (EPCs) by targeting GDF11 via activate SMAD2/3/FAK/Akt/eNOS pathway.Annals of translational medicine · 2019Article
- Role of fibroblast growth factor 23 and klotho cross talk in idiopathic pulmonary fibrosis.American journal of physiology. Lung cellular and molecular physiology · 2019Article
- PD-L1 on invasive fibroblasts drives fibrosis in a humanized model of idiopathic pulmonary fibrosis.JCI insight · 2019Article
- Developmental pathways in the pathogenesis of lung fibrosis.Molecular aspects of medicine · 2019Review
- Mechanisms for the Resolution of Organ Fibrosis.Physiology (Bethesda, Md.) · 2019Review
- TGF-β and the Tissue Microenvironment: Relevance in Fibrosis and Cancer.International journal of molecular sciences · 2018Review
- DHEA-induced ovarian hyperfibrosis is mediated by TGF-β signaling pathway.Journal of ovarian research · 2018Article
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Authors and funding
14 authors at 4 institutions in 2 countries.
Funding
Abstract
Alveolar epithelial cell (AEC) injury and apoptosis are prominent pathological features of idiopathic pulmonary fibrosis (IPF). There is evidence of AEC plasticity in lung injury repair response and in IPF. In this report, we explore the role of focal adhesion kinase (FAK) signaling in determining the fate of lung epithelial cells in response to transforming growth factor-β1 (TGF-β1). Rat type II alveolar epithelial cells (RLE-6TN) were treated with or without TGF-β1, and the expressions of mesenchymal markers, phenotype, and function were analyzed. Pharmacological protein kinase inhibitors were utilized to screen for SMAD-dependent and -independent pathways. SMAD and FAK signaling was analyzed using siRNA knockdown, inhibitors, and expression of a mutant construct of FAK. Apoptosis was measured using cleaved caspase-3 and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining. TGF-β1 induced the acquisition of mesenchymal markers, including α-smooth muscle actin, in RLE-6TN cells and enhanced the contraction of three-dimensional collagen gels. This phenotypical transition or plasticity, epithelial-myofibroblast plasticity (EMP), is dependent on SMAD3 and FAK signaling. FAK activation was found to be dependent on ALK5/SMAD3 signaling. We observed that TGF-β1 induces both EMP and apoptosis in the same cell culture system but not in the same cell. While blockade of SMAD signaling inhibited EMP, it had a minimal effect on apoptosis; in contrast, inhibition of FAK signaling markedly shifted to an apoptotic fate. The data support that FAK activation determines whether AECs undergo EMP vs. apoptosis in response to TGF-β1 stimulation. TGF-β1-induced EMP is FAK- dependent, whereas TGF-β1-induced apoptosis is favored when FAK signaling is inhibited.
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