TGF-β1-induced deposition of provisional extracellular matrix by tracheal basal cells promotes epithelial-to-mesenchymal transition in a c-Jun NH2-terminal kinase-1-dependent manner

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Fältnamn	Indikatorer	Metadata
000		03878naa a2200409 4500
001		oai:lup.lub.lu.se:adcfa663-7960-415c-b3c1-018c3a5c8e80
003		SwePub
008		180621s2018 \| \|\|\|\|\|\|\|\|\|\|\|000 \|\|eng\|
024	7	a https://lup.lub.lu.se/record/adcfa663-7960-415c-b3c1-018c3a5c8e802 URI
024	7	a https://doi.org/10.1152/ajplung.00053.20172 DOI
040		a (SwePub)lu
041		a engb eng
042		9 SwePub
072	7	a art2 swepub-publicationtype
072	7	a ref2 swepub-contenttype
100	1	a van der Velden, Jos L.u University of Vermont4 aut
245	1 0	a TGF-β1-induced deposition of provisional extracellular matrix by tracheal basal cells promotes epithelial-to-mesenchymal transition in a c-Jun NH2-terminal kinase-1-dependent manner
264	1	b American Physiological Society,c 2018
520		a Epithelial cells have been suggested as potential drivers of lung fibrosis, although the epithelial-dependent pathways that promote fibrogenesis remain unknown. Extracellular matrix is increasingly recognized as an environment that can drive cellular responses in various pulmonary diseases. In this study, we demonstrate that transforming growth factor-β1 (TGF-β1)-stimulated mouse tracheal basal (MTB) cells produce provisional matrix proteins in vitro, which initiate mesenchymal changes in subsequently freshly plated MTB cells via Rho kinase-and c-Jun NH2-terminal kinase (JNK1)-dependent processes. Repopulation of decellularized lung scaffolds, derived from mice with bleomycin-induced fibrosis or from patients with idiopathic pulmonary fibrosis, with wild-type MTB cells resulted in a loss of epithelial gene expression and augmentation of mesenchymal gene expression compared with cells seeded into decellularized normal lungs. In contrast, Jnk1-/- basal cells seeded into fibrotic lung scaffolds retained a robust epithelial expression profile, failed to induce mesenchymal genes, and differentiated into club cell secretory protein-expressing cells. This new paradigm wherein TGF-β1-induced extracellular matrix derived from MTB cells activates a JNK1-dependent mesenchymal program, which impedes subsequent normal epithelial cell homeostasis, provides a plausible scenario of chronic aberrant epithelial repair, thought to be critical in lung fibrogenesis. This study identifies JNK1 as a possible target for inhibition in settings wherein reepithelialization is desired.
650	7	a MEDICIN OCH HÄLSOVETENSKAPx Medicinska och farmaceutiska grundvetenskaperx Cell- och molekylärbiologi0 (SwePub)301082 hsv//swe
650	7	a MEDICAL AND HEALTH SCIENCESx Basic Medicinex Cell and Molecular Biology0 (SwePub)301082 hsv//eng
653		a ECM
653		a Epithelial
653		a Fibrosis
653		a JNK
700	1	a Wagner, Darcy E.u Lund University,Lunds universitet,Lungbioengineering och regeneration,Forskargrupper vid Lunds universitet,Lung Bioengineering and Regeneration,Lund University Research Groups,University of Vermont4 aut0 (Swepub:lu)da6033wa
700	1	a Lahue, Karolyn G.u University of Vermont4 aut
700	1	a Abdalla, Sarah T.u University of Vermont4 aut
700	1	a Lam, Ying Waiu University of Vermont4 aut
700	1	a Weiss, Daniel J.u University of Vermont4 aut
700	1	a Janssen-Heininger, Yvonne M.W.u University of Vermont4 aut
710	2	a University of Vermontb Lungbioengineering och regeneration4 org
773	0	t American Journal of Physiology: Lung Cellular and Molecular Physiologyd : American Physiological Societyg 314:6, s. 984-997q 314:6<984-997x 1522-1504x 1040-0605
856	4	u http://dx.doi.org/10.1152/ajplung.00053.2017y FULLTEXT
856	4	u https://journals.physiology.org/doi/pdf/10.1152/ajplung.00053.2017
856	4 8	u https://lup.lub.lu.se/record/adcfa663-7960-415c-b3c1-018c3a5c8e80
856	4 8	u https://doi.org/10.1152/ajplung.00053.2017

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