Epithelial to mesenchymal transition is increased in patients with COPD and induced by cigarette smoke

Milara, Javier; Peiró, Teresa; Serrano, Adela; Cortijo, Julio

doi:10.1136/thoraxjnl-2012-201761

Cited by 274 publications

(317 citation statements)

References 41 publications

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“…These results indicate that E-cadherin positive myofibroblasts are derived from the alveolar epithelial cells via EMT. Previous studies have demonstrated that epithelial cells undergoing EMT have decreased levels of E-cadherin and increased levels of α-SMA and collagen (Lekkerkerker et al, 2012;Milara et al, 2013). Therefore, our results suggest that sensitivity to MTX of alveolar epithelial cells is an important factor in the MTX-induced pulmonary fibrosis process.…”

Section: Figsupporting

confidence: 48%

Involvement of epithelial-mesenchymal transition in methotrexate-induced pulmonary fibrosis

et al. 2014

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-Epithelial-mesenchymal transition (EMT) plays a pivotal event in the development of pulmonary fibrosis. We have previously reported that methotrexate (MTX)-induced alveolar epithelial cell injury followed by pulmonary fibrosis as a result of the recruitment and proliferation of myofibroblasts. However, there is no data concerning whether EMT occurs in MTX-induced pulmonary fibrosis. In the present study, therefore, we investigated the expression of EMT markers such as E-cadherin, α-SMA, and vimentin by immunofluorescence analysis in mouse lung tissues after administration of MTX. We found that vimentin and α-SMA-positive cells of the MTX-induced pulmonary fibrosis were increased; on the other hand, E-cadherin was decreased, indicating that epithelial cells act as the main source of mesenchymal expansion. These results exhibited the down-regulation of E-cadherin expression and the up-regulation of α-smooth muscle actin (α-SMA) in primary mouse alveolar epithelial cells (MAECs) and A549 cell lines. Additionally, MTX-induced A549 cells exhibited an EMT-like phenotype accompanied by the elevation of the expression of interleukin-6 (IL-6) and transforming growth factor (TGF)-β1, as well as an enhancement of migration. All of these findings suggest that MTX-induced pulmonary fibrosis occurs via EMT.

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Section: Figsupporting

confidence: 48%

Involvement of epithelial-mesenchymal transition in methotrexate-induced pulmonary fibrosis

et al. 2014

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“…[35][36][37] Previous studies have demonstrated that epithelial cells undergoing EMT have decreased levels of epithelial cell markers such as E-cadherin and increased levels of myofibroblast markers such as a-SMA and mesenchymal cell marker collagen. 38,39 Our data that ATRA inhibited a-SMA and collagen expression and ATRA prevents lung fibrosis X Song et al increased the E-cadherin level support that ATRA might ameliorate lung fibrosis via suppressing EMT. To further study the effect of ATRA on EMT, we examined the expression of Snail and Twist, two most thoroughly studied transcription factors involved in EMT.…”

Section: Discussionmentioning

confidence: 90%

All-transretinoic acid ameliorates bleomycin-induced lung fibrosis by downregulating the TGF-β1/Smad3 signaling pathway in rats

Song

Liu

Xie

et al. 2013

Laboratory Investigation

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“…Elevated mesenchymal biomarkers including α-smooth muscle actin (α-SMA), vimentin and collagen type I, as well as decreased epithelial biomarkers E-cadherin, ZO-1 and cytokeratin have been observed in small airway epithelium from COPD patients. Moreover, EMT features of the bronchial epithelium are associated with the severity of airway limitation (3,4), suggesting the involvement of EMT in progression of COPD. The induction of EMT in human bronchial epithelial (HBE) cells was also observed upon the stimulation with cigarette smoke or TGF-β1 in vitro (3,5).…”

Section: Introductionmentioning

confidence: 99%

“…Moreover, EMT features of the bronchial epithelium are associated with the severity of airway limitation (3,4), suggesting the involvement of EMT in progression of COPD. The induction of EMT in human bronchial epithelial (HBE) cells was also observed upon the stimulation with cigarette smoke or TGF-β1 in vitro (3,5). Taken together, these findings indicate the involvement of EMT in airway remodelling of COPD.…”

Section: Introductionmentioning

confidence: 99%

“…The narrowing of small airways leads to increased peripheral airway resistance of patients with COPD (1). Although mechanisms of airway remodelling in COPD are not yet clearly elucidated, epithelial-mesenchymal transition (EMT) has been implicated in this process (2,3). During EMT, airway epithelial cells can acquire a mesenchymal phenotype and transform into fibroblasts/myofibroblasts, which produce excessive ECM proteins.…”

Section: Introductionmentioning

confidence: 99%

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Overexpression of farnesoid X receptor in small airways contributes to epithelial to mesenchymal transition and COX-2 expression in chronic obstructive pulmonary disease

Bi¹,

You²,

Xue³

et al. 2016

J. Thorac. Dis.

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Background: Epithelial-mesenchymal transition (EMT) and cyclooxygenase-2 (COX-2) contribute to airway remodelling and inflammation in chronic obstructive pulmonary disease (COPD). Recent data suggest that the farnesoid X receptor (FXR), a nuclear receptor traditionally considered as bile acid-activated receptor, is also expressed in non-classical bile acids target tissues with novel functions beyond regulating bile acid homeostasis. This study aimed to investigate the potential role of FXR in the development of COPD, as well as factors that affect FXR expression. Conclusions: Overexpression of FXR in small airway may contribute to airway remodelling and inflammation in COPD by regulating EMT and COX-2 expression.

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Epithelial to mesenchymal transition is increased in patients with COPD and induced by cigarette smoke

Cited by 274 publications

References 41 publications

Involvement of epithelial-mesenchymal transition in methotrexate-induced pulmonary fibrosis

Involvement of epithelial-mesenchymal transition in methotrexate-induced pulmonary fibrosis

All-transretinoic acid ameliorates bleomycin-induced lung fibrosis by downregulating the TGF-β1/Smad3 signaling pathway in rats

Overexpression of farnesoid X receptor in small airways contributes to epithelial to mesenchymal transition and COX-2 expression in chronic obstructive pulmonary disease

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