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Maldonado, M.* ; Salgado-Aguayo, A.* ; Herrera, I.* ; Cabrera, S.* ; Ortíz-Quintero, B.* ; Staab-Weijnitz, C.A. ; Eickelberg, O. ; Ramírez, R.* ; Manicone, A.M.* ; Selman, M.* ; Pardo, A.*

Upregulation and nuclear location of MMP28 in alveolar epithelium of idiopathic pulmonary fibrosis.

Am. J. Respir. Cell Mol. Biol. 59, 77-86 (2018)
Publ. Version/Full Text Postprint DOI PMC
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Idiopathic pulmonary fibrosis (IPF) is a chronic and progressive aging-associated disease of unknown etiology. A growing body of evidence indicates that aberrant activated alveolar epithelial cells induce the expansion and activation of the fibroblast population, leading to the destruction of the lung architecture. Some matrix metalloproteinases (MMPs) are upregulated in IPF, indicating that they may be important in the pathogenesis and/or progression of IPF. In the present study, we examined the expression of MMP28 in this disease and evaluated its functional effects in two alveolar epithelial cell lines and in human primary bronchial epithelial cells. We found that the enzyme is expressed in bronchial (apical and cytoplasmic localization) and alveolar (cytoplasmic and nuclear localization) epithelial cells in two different groups of patients with IPF. In vitro MMP28 epithelial silencing decreased the proliferation rate and delayed wound closing, whereas overexpression showed opposite effects, protecting from apoptosis and enhanced epithelial-mesenchymal transition. Our findings demonstrate that MMP28is upregulated in epithelial cells from IPF lungs, where it may play a role in increasing the proliferative and migratory phenotype in a catalysis-dependent manner.
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Publication type Article: Journal article
Document type Scientific Article
Corresponding Author
Keywords Matrix Metalloproteinase ; Lung Epithelial Cells ; Idiopathic Pulmonary Fibrosis; Human Matrix-metalloproteinase; Gene-expression; Mmp-28; Pathogenesis; Apoptosis; Epilysin; Cells; Carcinoma; Disease; Humans
ISSN (print) / ISBN 1044-1549
e-ISSN 1535-4989
Journal American Journal of Respiratory Cell and Molecular Biology
Quellenangaben Volume: 59, Issue: 1, Pages: 77-86 Article Number: , Supplement: ,
Publisher American Thoracic Society
Publishing Place 25 Broadway, 18 Fl, New York, Ny 10004 Usa
Non-patent literature Publications
Reviewing status Peer reviewed
Institute(s) Lung Health and Immunity (LHI)