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Role of MUC1 in idiopathic pulmonary fibrosis: mechanistic insights

Beatriz Ballester, Ines Roger, Sonia Contreras, Paula Montero, Javier Milara
European Respiratory Journal 2017 50: PA4889; DOI: 10.1183/1393003.congress-2017.PA4889
Beatriz Ballester
1Pharmacology Department, University of Valencia, Valencia, Spain
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Ines Roger
2Centro de Investigación Biomédica en Red de Enfermedades Respiratorias (CIBERES, Madrid, Spain
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Sonia Contreras
1Pharmacology Department, University of Valencia, Valencia, Spain
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Paula Montero
1Pharmacology Department, University of Valencia, Valencia, Spain
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Javier Milara
3Pharmacy Department, General Hospital of Valencia, Valencia, Spain
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Abstract

Background:

Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive and irreversible form of fibrotic interstitial lung disease. MUC1, a membrane-bound O-glycoprotein, is considered as oncogenic molecule by altering signaling pathways involved in cellular processes related to IPF. In previous studies we have observed an up-regulation of MUC1 and its phosphorylated forms in IPF lung tissue. However the exact participation of MUC1 in IPF is currently unknown.

Objective: To analyze the mechanism of MUC1-induced lung fibrosis in different cellular and animal models of IPF.

Methods: The intracellular mechanism of MUC1 was evaluated by western blot, immunoprecipation and immunofluorescence in alveolar type II A549 and fibroblast MRC5, and IPF primary alveolar type II epithelial cells and lung fibroblasts. Cells were stimulated with TGFβ1. Lung tissue from human healthy/IPF and bleomycin-induced IPF mice wild type/ knockout MUC1 (KO-MUC1) was analyzed to explore MUC1 intracellular interactions by immunofluorescence.

Results: Western blot indicated that TGFβ1 activated β-catenin and p-Smad2/3, which phosphorylated and activated MUC1 cytoplasmic tail (CT) at 1224 and 1229 treonin and tirosin residues. Immunoprecipitation and immunofluorescence studies showed that the multi-protein complex among pSmad2/3, β-catenin and MUC1-CT migrated into the nucleus to activate fibrotic genes in human cells and human and animal lung tissue. Unlike wild type mice, KO-MUC1 mice were protected against IPF, improving lung function, survival and fibrotic lung tissue remodeling.

Conclusions: MUC1-CT collaborates with TGFβ1 to induce IPF progression. Therefore, pharmacologic targeting of MUC1-CT may be a promising option for the treatment of IPF.

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Role of MUC1 in idiopathic pulmonary fibrosis: mechanistic insights
Beatriz Ballester, Ines Roger, Sonia Contreras, Paula Montero, Javier Milara
European Respiratory Journal Sep 2017, 50 (suppl 61) PA4889; DOI: 10.1183/1393003.congress-2017.PA4889

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Role of MUC1 in idiopathic pulmonary fibrosis: mechanistic insights
Beatriz Ballester, Ines Roger, Sonia Contreras, Paula Montero, Javier Milara
European Respiratory Journal Sep 2017, 50 (suppl 61) PA4889; DOI: 10.1183/1393003.congress-2017.PA4889
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