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Epithelial-mesenchymal transition contributes to pulmonary fibrosis via aberrant epithelial/fibroblastic cross-talk

Epithelial-mesenchymal transition contributes to pulmonary fibrosis via aberrant epithelial/fibroblastic cross-talk
Epithelial-mesenchymal transition contributes to pulmonary fibrosis via aberrant epithelial/fibroblastic cross-talk
Idiopathic pulmonary fibrosis (IPF) is the prototypic progressive fibrotic interstitial lung disease. Median survival is only 3 years, and treatment options are limited. IPF is thought to be a result of a combination of genetic and environmental factors with repetitive micro-injuries to alveolar epithelial cells playing a central role. IPF is characterised by aberrant extra cellular matrix (ECM) deposition by activated myofibroblasts. Epithelial-mesenchymal transition (EMT) is a process where polarised
epithelial cells undergo molecular changes allowing them to gain a mesenchymal phenotype, with a subsequent enhanced ability to produce ECM components and increased migration and/or invasion. The source of myofibroblasts in IPF has been debated for many years, and EMT has been proposed as a source of these cells. However, lineage tracing in transgenic mice suggests the contribution of epithelial cells, which have undergone EMT, to the fibroblast population may be negligible. Instead, recent findings suggest that alveolar epithelial type II (ATII) cells undergoing EMT promote a profibrotic microenvironment through paracrine signalling activating local fibroblasts. This review paper explores the contribution of ATII cells, which have undergone EMT, in the context of pulmonary
fibrosis.
Hill, Charlotte
6d1cfed3-11b1-48af-b171-b8726ab673eb
Jones, Mark
a6fd492e-058e-4e84-a486-34c6035429c1
Davies, Donna
7de8fdc7-3640-4e3a-aa91-d0e03f990c38
Wang, Yihua
f5044a95-60a7-42d2-87d6-5f1f789e3a7e
Hill, Charlotte
6d1cfed3-11b1-48af-b171-b8726ab673eb
Jones, Mark
a6fd492e-058e-4e84-a486-34c6035429c1
Davies, Donna
7de8fdc7-3640-4e3a-aa91-d0e03f990c38
Wang, Yihua
f5044a95-60a7-42d2-87d6-5f1f789e3a7e

Hill, Charlotte, Jones, Mark, Davies, Donna and Wang, Yihua (2019) Epithelial-mesenchymal transition contributes to pulmonary fibrosis via aberrant epithelial/fibroblastic cross-talk. Journal of Lung Health and Diseases. (In Press)

Record type: Review

Abstract

Idiopathic pulmonary fibrosis (IPF) is the prototypic progressive fibrotic interstitial lung disease. Median survival is only 3 years, and treatment options are limited. IPF is thought to be a result of a combination of genetic and environmental factors with repetitive micro-injuries to alveolar epithelial cells playing a central role. IPF is characterised by aberrant extra cellular matrix (ECM) deposition by activated myofibroblasts. Epithelial-mesenchymal transition (EMT) is a process where polarised
epithelial cells undergo molecular changes allowing them to gain a mesenchymal phenotype, with a subsequent enhanced ability to produce ECM components and increased migration and/or invasion. The source of myofibroblasts in IPF has been debated for many years, and EMT has been proposed as a source of these cells. However, lineage tracing in transgenic mice suggests the contribution of epithelial cells, which have undergone EMT, to the fibroblast population may be negligible. Instead, recent findings suggest that alveolar epithelial type II (ATII) cells undergoing EMT promote a profibrotic microenvironment through paracrine signalling activating local fibroblasts. This review paper explores the contribution of ATII cells, which have undergone EMT, in the context of pulmonary
fibrosis.

Text
Epithelial-mesenchymal transition contributes to pulmonary fibrosis via aberrant epithelial-fibroblastic cross-talk - Accepted Manuscript
Restricted to Repository staff only until 3 June 2019.
Available under License Creative Commons Attribution.
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Accepted/In Press date: 3 April 2019

Identifiers

Local EPrints ID: 429970
URI: https://eprints.soton.ac.uk/id/eprint/429970
PURE UUID: 1e72f299-2324-400f-85ba-4ca4f801f894
ORCID for Yihua Wang: ORCID iD orcid.org/0000-0001-5561-0648

Catalogue record

Date deposited: 09 Apr 2019 16:30
Last modified: 02 May 2019 00:30

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