AHR:IKAROS Interaction Promotes Platelet Biogenesis in Response to SR1

In vitro, the differentiation of megakaryocytes (MKs) is improved by aryl-hydrocarbon receptor (AHR) antagonists such as StemRegenin 1 (SR1), an effect physiologically recapitulated presence stromal mesenchymal cells (MSC). This inhibition promotes amplification a CD34+CD41low population able to mature MKs with high capacity for platelet production. this short report, we showed that emergence thrombocytogenic precursors and enhancement production triggered SR1 involved IKAROS. The downregulation/inhibition IKAROS (shRNA or lenalidomide) significantly reduced SR1-induced population, suggesting crosstalk between AHR Interestingly, using proximity ligation assay, could demonstrate physical interaction was also observed in megakaryocytic differentiated MSCs. conclusion, our study revealed previously unknown AHR/ -dependent pathway which prompted expansion precursors. AHR- dependent checkpoint controlling MK maturation opens new perspectives engineering.