Please use this identifier to cite or link to this item: http://hdl.handle.net/10397/80448
Title: M2 macrophages promote myofibroblast differentiation of LR-MSCs and are associated with pulmonary fibrogenesis
Authors: Hou, JW
Shi, JY
Chen, L
Lv, ZY
Chen, X
Cao, HH
Xiang, Z 
Han, XD
Keywords: Idiopathic pulmonary fibrosis (IPF)
M2 macrophages
Lung resident mesenchymal stem cells (LR-MSCs)
Myofibroblast differentiation
Issue Date: 2018
Publisher: BioMed Central
Source: Cell communication and signaling, 23 Nov. 2018, v. 16, 89, p. 1-14 How to cite?
Journal: Cell communication and signaling 
Abstract: Background: Idiopathic pulmonary fibrosis (IPF) is a devastating disease characterized by the histopathological pattern of usual interstitial pneumonia and is associated with a high mortality rate. Recently, lung resident mesenchymal stem cells (LR-MSCs) have been identified as an important contributor to myofibroblast activation in pulmonary fibrosis. Macrophages are also believed to play a critical role in pulmonary fibrosis. However, the underlying connections between LR-MSCs and macrophages in the pathogenesis of pulmonary fibrosis are still elusive.
Methods: In this study, we investigated the interaction between LR-MSCs and macrophages using a bleomycin-induced mouse pulmonary fibrosis model and a coculture system.
Results: Here, we show that blocking pulmonary macrophage infiltration attenuated bleomycin-induced pulmonary fibrosis. In addition, as determined by flow cytometry, we discovered that the recruited macrophages in fibrotic lungs of bleomycin-treated mice were mainly M2 macrophages. In particular, we found that M2, rather than M1 macrophages, promoted myofibroblast differentiation of LR-MSCs. Moreover, we demonstrated that suppression of the Wnt/-catenin signaling pathway could attenuate myofibroblast differentiation of LR-MSCs induced by M2 macrophages and bleomycin-induced pulmonary fibrosis. Tissue samples from IPF patients confirmed the infiltration of M2 macrophages and activation of Wnt/-catenin signaling pathway.
Conclusion: In summary, this study furthered our understanding of the pulmonary fibrosis pathogenesis and highlighted M2 macrophages as a critical target for treating pulmonary fibrosis.
URI: http://hdl.handle.net/10397/80448
EISSN: 1478-811X
DOI: 10.1186/s12964-018-0300-8
Rights: © The Author(s). 2018 Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver(http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
The following publication Hou, J. W., Shi, J. Y., Chen, L., Lv, Z. Y., Chen, X., Cao, H. H., . . . Han, X. D. (2018). M2 macrophages promote myofibroblast differentiation of LR-MSCs and are associated with pulmonary fibrogenesis. Cell Communication and Signaling, 16, 89, 1-14 is available at https://dx.doi.org/10.1186/s12964-018-0300-8
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