Wnt/β-catenin signaling regulates lipopolysaccharide-altered polarizations of RAW264.7 cells and alveolar macrophages in mouse lungs
Wnt/β-catenin signaling regulates lipopolysaccharide-altered polarizations of RAW264.7 cells and alveolar macrophages in mouse lungs
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Wnt/β-连环蛋白信号调节脂多糖改变小鼠肺中 RAW264.7 细胞和肺泡巨噬细胞的极化
DOI:
10.1177/20587392211059362
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发表时间:
2021-01
影响因子:
0.7
通讯作者:
Xiaoming Liu
中科院分区:
文献类型:
--
作者:
Jiali Yang;Ying Wang;D;an Yang;Jia Ma;Shuang Wu;Qian Cai;Jing Xue;Chao Yuan;Jing Wang;Xiaoming Liu
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.
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影响因子:
7.6
作者:
Liu F;Millar SE
通讯作者:
Millar SE
影响因子:
9
作者:
Yang Y;Ye YC;Chen Y;Zhao JL;Gao CC;Han H;Liu WC;Qin HY
通讯作者:
Qin HY
影响因子:
3.7
作者:
Cosín-Roger J;Ortiz-Masiá D;Calatayud S;Hernández C;Alvarez A;Hinojosa J;Esplugues JV;Barrachina MD
通讯作者:
Barrachina MD
影响因子:
30.5
作者:
Piccolo V;Curina A;Genua M;Ghisletti S;Simonatto M;Sabò A;Amati B;Ostuni R;Natoli G
通讯作者:
Natoli G
影响因子:
12.8
作者:
Song, Mi-Young;Kim, Sang Hoon;Park, Byung-Hyun
通讯作者:
Park, Byung-Hyun