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Fig. 2 | Respiratory Research

Fig. 2

From: Acute cigarette smoke exposure activates apoptotic and inflammatory programs but a second stimulus is required to induce epithelial to mesenchymal transition in COPD epithelium

Fig. 2

TGFβ1 but not CSE drives a mesenchymal phenotype in lung epithelial cells. Exposure of NHBE (a-c) or COPD-AEC (D-F) cells to TGF β1 (10 ng/ml) decreased E-cadherin and increased EDA-Fn expression (A-C). Exposure to CSE (5%) did not impact on E-cadherin expression in the presence or absence of TGF-β1 (a, b), but at a high concentration (20%) did reduce TGFβ1-induced EDA-Fn expression (a, c). COPD-AEC were resistant to EMT. Exposure of AEC from COPD patients (Lonza) to TGFβ1 had minimal effect on E-Cadherin expression (d, e) although it did induce EDA-Fn expression (d, f). Exposure to CSE (5%) did not impact E-Cadherin (d, e) or EDA-Fn (d, f) expression in the presence or absence of TGF-β1. Representative western blots from NHBE donor cells (a) or COPD donor cells (d), shown alongside densitometry from 3 NHBE donors (b, c) or 1 COPD donor repeated 3 times (e, f), protein levels normalised to β-tubulin loading control

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Respiratory Research

ISSN: 1465-993X

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