Lack of epithelial-to-mesenchymal transition induction in two bronchial epithelial cell lines after alpha and gamma irradiation

Abstract

Abstract:The induction of epithelial-to-mesenchymal transition (EMT) in human lung epithelial cell lines was investigated after α-particle and γ-radiation exposures. We applied TGF-β treatment of cells as positive EMT-controls and tested in parallel if radiation has a potentiating effect on the EMT induction. BEAS-2B and HBEC-3KT cells were irradiated with 5.4 MeV α-particles or γ-rays ( 60 Co, 1.13-1.15 Gy/min) with or without of TGF-β. The cells were harvested three days post treatment and the EMT markers vimentin, fibronectin and E-cadherin were analysed by immunofluorescence staining and Western blotting. The TGF-β treatment-induced EMT in both cell lines in the applied concentrations. We could not prove any clear EMT induction with low or moderate doses of α-particles and γ-rays. No significant additive effect with radiation and TGF-β was observed. We suggest that there might be a different mechanism induced by radiation in bronchial cells after radon and medical exposures that does not involve direct EMT changes.

Presence of Stromal Cells Enhances Epithelial-to-Mesenchymal Transition (EMT) Induction in Lung Bronchial Epithelium after Protracted Exposure to Oxidative Stress of Gamma Radiation

“…We observed a similar trend in our experiments for oxidative stress induction in the epithelial cell line (BEAS-2B) at 0.1 Gy. Earlier, we detected an increase in the TGF- β levels in the MRC-9 fibroblasts after acute exposure to doses of 0.1-2 Gy [34]. Other scientists have reported a significant role of TGF- β in the activation of oxidative stress response, especially in myofibroblastic cells during their invasive transformation [40].…”

“…In our prestudies with acute radiation exposures, some of the classical features of the EMT were not affected, although some of the markers or phenotypic features were changed. For example, the ZO-1 and β -catenin expression were not affected (data not shown), while the vimentin and E-cadherin were, respectively, up- or downregulated [34]. In the earlier study, we could not prove any clear EMT induction with low or moderate doses of α -particles and γ -rays.…”

“…The cell lines were immunostained for vimentin (BEAS-2B) and E-cadherin (HBEC-3KT). These markers were selected after the two lines were screened for sensitivity to EMT-inducing stimuli and EMT marker expression levels [34]. BEAS-2B cells showed significant changes in vimentin expression and HBEC-3KT in E-cadherin expression, and these two markers were used in [34] and further as the most sensitive.…”

The Potential Role of Bile Acids in Acquired Laryngotracheal Stenosis

“…Further studies have demonstrated links between aspiration of gastric refluxate and progression of a number of lower airway fibrotic diseases, including cystic fibrosis, lung transplant rejection, chronic obstructive pulmonary disease, and pulmonary fibrosis . Furthermore, EMT is strongly implicated in laryngotracheal malignancies, and further investigation of the role of bile acids in these cancers is needed …”

“…12,18 Furthermore, EMT is strongly implicated in laryngotracheal malignancies, and further investigation of the role of bile acids in these cancers is needed. 22 Cells were also stimulated with 5 ng/mL TGF-b1 as a positive control in our study. This followed preliminary work in which we established that 5 ng/mL was an optimum concentration of TGF-b1 to stimulate primary PTECs and cell lines.…”