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• W2886602181 abstract "Macrophage-epithelial cross-talk regulates cell cycle progression and represents an important factor in rescuing epithelial cells from cell cycle arrest in order to maintain a healthy epithelial phenotype. However, the underlying mechanisms are still not well defined. We provide evidence that macrophage-secreted lipocalin-2 (Lcn-2) plays a key role during this process. In a co-culture setup using cell cycle arrested NRK52e renal epithelial cells and primary bone marrow-derived macrophages, Lcn-2 restores proliferation through inhibition of peroxisome proliferator-activated receptor (PPAR)-γ. Lcn-2 overexpression in macrophages overcomes epithelial cell cycle arrest and enhances epithelial markers via megalin and the downstream activation of PI3K/Akt signalling pathway, whereas a knockdown of Lcn-2 in macrophages prevented this effect. Our results show that macrophage-secreting Lcn-2 is crucial in rescuing epithelial cells from cell cycle arrest and in promoting epithelial proliferation.Macrophage-epithelial crosstalk regulates cell cycle progression and is essential for the maintenance of a healthy epithelial phenotype. In the present work, the authors show that macrophage-secreted lipocalin-2 is crucial in rescuing epithelial cells from cell cycle arrest and in promoting epithelial proliferation through inhibition of peroxisome proliferator-activated receptor (PPAR)-γ. Lipocalin-2 maintains the epithelial cytoskeleton structure via megalin and downstream activation of thePI3K/AKT signaling pathway." @default.
• W2886602181 created "2018-08-22" @default.
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• W2886602181 date "2018-11-01" @default.
• W2886602181 modified "2023-10-09" @default.
• W2886602181 title "Lipocalin-2 abrogates epithelial cell cycle arrest by PPARγ inhibition" @default.
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• W2886602181 doi "https://doi.org/10.1038/s41374-018-0098-4" @default.
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