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Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Cell+Death+Dis 2017 ; 8 (10): e3105- Nephropedia Template TP
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RANKL-mediated harmonious dialogue between fetus and mother guarantees smooth gestation by inducing decidual M2 macrophage polarization #MMPMID29022922
Meng YH; Zhou WJ; Jin LP; Liu LB; Chang KK; Mei J; Li H; Wang J; Li DJ; Li MQ
Cell Death Dis 2017[Oct]; 8 (10): e3105- PMID29022922show ga
Decidual macrophages (dM?) contribute to maternal?fetal tolerance. However, the mechanism of dM? differentiation during pregnancy is still largely unknown. Here, we report that receptor activator for nuclear factor-? B ligand (RANKL), secreted by human embryonic trophoblasts and maternal decidual stromal cells (DSCs), polarizes dM? toward a M2 phenotype. This polarization is mediated through activation of Akt/signal transducer and activator of transcription 6 (STAT6) signaling, which is associated with the upregulation of histone H3 lysine-27 demethylase Jmjd3 and IRF4 in dM?. Such differentiated dM? can induce a Th2 bias that promotes maternal?fetal tolerance. Impaired expression of RANKL leads to dysfunction of dM? in vivo and increased rates of fetal loss in mice. Transfer of RANK+M? reverses mouse fetal loss induced by M? depletion. Compared with normal pregnancy, there are abnormally low levels of RANKL/RANK in villi and decidua from miscarriage patients. These results suggest that RANKL is a pivotal regulator of maternal?fetal tolerance by licensing dM? to ensure a successful pregnancy outcome. This observation provides a scientific basis on which a potential therapeutic strategy can be targeted to prevent pregnancy loss.