Ltd
Ltd. no effect on normal hematopoiesis. Protein analysis showed that EC-derived SEVs contained a high level of ANGPTL2, which accelerated leukemia progression via binding to the LILRB2 receptor. Moreover, ANGPTL2-SEVs released from ECs were governed by VPS33B. Importantly, ANGPTL2-SEVs were also required for main human AML cell maintenance. These findings demonstrate a role of niche-specific SEVs in malignancy development and suggest targeting of ANGPTL2-SEVs from ECs as a potential strategy to interfere with certain types of AML. = 3). Ctrl, control. The data represent the means SD; ***< 0.001, Students test. Experiments were conducted 2 times for validation. Reducing EC-derived SEV secretion prolongs survival in AML mice. To determine whether is required for SEV release by the different niche cells, we knocked down the gene with shRNA lentivirus in main…