Lipocalin-2 abrogates epithelial cell cycle arrest by PPARγ inhibition
2018
Macrophage-epithelial cross-talk regulates
cell cycleprogression and represents an important factor in rescuing epithelial cells from
cell cyclearrest 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 cyclearrested 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 cyclearrest 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 cyclearrest and in promoting epithelial proliferation.
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