Wnt/β-catenin signaling regulates lipopolysaccharide-altered polarizations of RAW264.7 cells and alveolar macrophages in mouse lungs

Introduction Macrophages are capable of exerting both proinflammatory and anti-inflammatory functions in response to distinct environmental stimuli, by polarizing into classically inflammatory state (M1) and anti-inflammatory phenotype (M2), respectively. The Wnt/β-catenin signaling plays an importa...

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Autores principales: Jiali Yang, Ying Wang, Dandan Yang, Jia Ma, Shuang Wu, Qian Cai, Jing Xue, Chao Yuan, Jing Wang, Xiaoming Liu
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Publicado: SAGE Publishing 2021
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Acceso en línea:https://doaj.org/article/be4060b9588b40b680c100c9218e9727
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spelling oai:doaj.org-article:be4060b9588b40b680c100c9218e97272021-12-01T02:04:09ZWnt/β-catenin signaling regulates lipopolysaccharide-altered polarizations of RAW264.7 cells and alveolar macrophages in mouse lungs2058-739210.1177/20587392211059362https://doaj.org/article/be4060b9588b40b680c100c9218e97272021-11-01T00:00:00Zhttps://doi.org/10.1177/20587392211059362https://doaj.org/toc/2058-7392Introduction Macrophages are capable of exerting both proinflammatory and anti-inflammatory functions in response to distinct environmental stimuli, by polarizing into classically inflammatory state (M1) and anti-inflammatory phenotype (M2), respectively. The Wnt/β-catenin signaling plays an important role in the tissue homeostasis and immune regulations, including the macrophage polarizations. However, the molecular mechanism of Wnt/β-catenin signaling in regulating alveolar macrophage polarization in an inflammatory state remains unclear. Methods The Wnt/β-catenin signaling-altered phenotypes of murine macrophage-like RAW264.7 cells in vitro and alveolar macrophage in vivo in both of naïve and lipopolysaccharide-induced inflammation states were accessed by immunoblotting and immunostaining assays. Results The activation of Wnt/β-catenin signaling inhibited macrophage M1 polarization, but promoted alternative M2 polarization in murine RAW264.7 cells under a naïve state. Interestingly, in an LPS-induced inflammation condition, the enhanced Wnt/β-catenin activity suppressed both M1 and M2 polarizations in RAW264.7 cells in vitro, and primary alveolar macrophages of LPS-challenged mice in vivo . Molecular analysis further demonstrated an involvement of Stat signing in regulating Wnt/β-catenin signaling-altered polarizations in mouse alveolar macrophages. Conclusion These results suggest a mechanism by which Wnt/β-catenin signaling modulates macrophage polarization in an inflammation state by regulating the Stat signaling pathway.Jiali YangYing WangDandan YangJia MaShuang WuQian CaiJing XueChao YuanJing WangXiaoming LiuSAGE PublishingarticleMedicineRENEuropean Journal of Inflammation, Vol 19 (2021)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
spellingShingle Medicine
R
Jiali Yang
Ying Wang
Dandan Yang
Jia Ma
Shuang Wu
Qian Cai
Jing Xue
Chao Yuan
Jing Wang
Xiaoming Liu
Wnt/β-catenin signaling regulates lipopolysaccharide-altered polarizations of RAW264.7 cells and alveolar macrophages in mouse lungs
description Introduction Macrophages are capable of exerting both proinflammatory and anti-inflammatory functions in response to distinct environmental stimuli, by polarizing into classically inflammatory state (M1) and anti-inflammatory phenotype (M2), respectively. The Wnt/β-catenin signaling plays an important role in the tissue homeostasis and immune regulations, including the macrophage polarizations. However, the molecular mechanism of Wnt/β-catenin signaling in regulating alveolar macrophage polarization in an inflammatory state remains unclear. Methods The Wnt/β-catenin signaling-altered phenotypes of murine macrophage-like RAW264.7 cells in vitro and alveolar macrophage in vivo in both of naïve and lipopolysaccharide-induced inflammation states were accessed by immunoblotting and immunostaining assays. Results The activation of Wnt/β-catenin signaling inhibited macrophage M1 polarization, but promoted alternative M2 polarization in murine RAW264.7 cells under a naïve state. Interestingly, in an LPS-induced inflammation condition, the enhanced Wnt/β-catenin activity suppressed both M1 and M2 polarizations in RAW264.7 cells in vitro, and primary alveolar macrophages of LPS-challenged mice in vivo . Molecular analysis further demonstrated an involvement of Stat signing in regulating Wnt/β-catenin signaling-altered polarizations in mouse alveolar macrophages. Conclusion These results suggest a mechanism by which Wnt/β-catenin signaling modulates macrophage polarization in an inflammation state by regulating the Stat signaling pathway.
format article
author Jiali Yang
Ying Wang
Dandan Yang
Jia Ma
Shuang Wu
Qian Cai
Jing Xue
Chao Yuan
Jing Wang
Xiaoming Liu
author_facet Jiali Yang
Ying Wang
Dandan Yang
Jia Ma
Shuang Wu
Qian Cai
Jing Xue
Chao Yuan
Jing Wang
Xiaoming Liu
author_sort Jiali Yang
title Wnt/β-catenin signaling regulates lipopolysaccharide-altered polarizations of RAW264.7 cells and alveolar macrophages in mouse lungs
title_short Wnt/β-catenin signaling regulates lipopolysaccharide-altered polarizations of RAW264.7 cells and alveolar macrophages in mouse lungs
title_full Wnt/β-catenin signaling regulates lipopolysaccharide-altered polarizations of RAW264.7 cells and alveolar macrophages in mouse lungs
title_fullStr Wnt/β-catenin signaling regulates lipopolysaccharide-altered polarizations of RAW264.7 cells and alveolar macrophages in mouse lungs
title_full_unstemmed Wnt/β-catenin signaling regulates lipopolysaccharide-altered polarizations of RAW264.7 cells and alveolar macrophages in mouse lungs
title_sort wnt/β-catenin signaling regulates lipopolysaccharide-altered polarizations of raw264.7 cells and alveolar macrophages in mouse lungs
publisher SAGE Publishing
publishDate 2021
url https://doaj.org/article/be4060b9588b40b680c100c9218e9727
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