ArticleIn vivo (Athens, Greece)
Antagonistic Effect of Erythropoietin Receptor Signaling in Macrophages and Type II Alveolar Epithelial Cells on Pulmonary Fibrosis in Mice.
Article in In vivo (Athens, Greece). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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6 authors.
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Abstract
BACKGROUND/
aimAlthough stimulation of erythropoietin receptor (EPOR) signaling demonstrates cytoprotective effects-including anti-apoptosis, pro-proliferation, and promotion of inflammation resolution-in various disease models, its alterations and specific role in the process of pulmonary fibrosis are still not well understood. The study aimed at investigating the changes of lung EPOR signal in pulmonary fibrosis and the effect of different cell EPOR signal on pulmonary fibrosis. MATERIALS AND
methodsIn a bleomycin-induced C57BL/6J mice model, fibrosis was assessed
resultsLung overall EPOR expression decreased after fibrosis. Type II alveolar epithelial cells and macrophages showed the highest baseline EPOR expression, which declined post-fibrosis. CM from BLM+EPO-treated MLE-12 cells inhibited fibroblast activation, while media from PMs and C166 cells promoted it. Direct EPOR activation in fibroblasts enhanced their activation. MΦ-EPOR
conclusionEPOR signaling in macrophages and type II alveolar epithelial cells exerts opposing effects on pulmonary fibrosis, with targeted activation EPOR signaling in alveolar epithelial cells representing a potential therapeutic strategy.
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