Acute myeloid leukemia (AML) is a malignant clonal disease derived from hematopoietic stem/progenitor cell. Leukemia blasts cause extensive hypoxia of bone marrow (BM), which lead to disorder and remodeling of BM niche, thereby becoming “leukemic niche” to support the development and drug-resistance of AML as well as the maintenance of normal hematopoietic stem cells. In this study, the biological characteristics (such as self-renewal, apoptosis, migration, autocrine) and function (vascularization) of mesenchymal stem cells (MSCs) and human umbilical artery endothelial cells (HUAECs) that make up BM arteriolar niche in simulated hypoxia AML context were investigated. It was found that moderate hypoxia enhanced the viability of the arteriolar niche cells, but severe hypoxia of AML BM resulted in the damage of arteriolar niche cells and the disorder of vascular cytokines C-X-C motif chemokine ligand 6 (CXCL6). The dynamic changes of CXCL6 in the system as well as its anti-apoptotic and promoting angiogenic effects suggested that CXCL6 played an important role in the remodeling of BM arteriolar niche in AML. Taking advantage of CXCL6 can save the damaged MSCs and HUAECs, which is the hope of rescuing arteriolar niche. It is suggested that CXCL6 may be an assistant strategy for microenvironment targeted therapy of AML.

急性髓系白血病（AML）是一种源自造血干/祖细胞的恶性克隆性疾病。白血病原始细胞引起骨髓（BM）的广泛缺氧，导致BM生态位的紊乱和重塑，从而成为支持AML的发展和耐药性以及维持正常造血干细胞的“白血病生态位”。在这项研究中，模拟缺氧中构成 BM 小动脉生态位的间充质干细胞 (MSCs) 和人脐动脉内皮细胞 (HUAECs) 的生物学特性（如自我更新、凋亡、迁移、自分泌）和功能（血管化）研究了 AML 的背景。发现中度缺氧增强了小动脉生态位细胞的活力，但AML BM的严重缺氧导致小动脉生态位细胞损伤和血管细胞因子CXC基序趋化因子配体6（CXCL6）的紊乱。CXCL6在系统中的动态变化及其抗凋亡和促血管生成作用提示CXCL6在AML中BM小动脉生态位的重塑中发挥了重要作用。利用CXCL6可以挽救受损的MSCs和HUAECs，是挽救小动脉生态位的希望。提示CXCL6可能是AML微环境靶向治疗的辅助策略。利用CXCL6可以挽救受损的MSCs和HUAECs，是挽救小动脉生态位的希望。提示CXCL6可能是AML微环境靶向治疗的辅助策略。利用CXCL6可以挽救受损的MSCs和HUAECs，是挽救小动脉生态位的希望。提示CXCL6可能是AML微环境靶向治疗的辅助策略。