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内皮衍生的小细胞外囊泡支持B细胞急性淋巴细胞白血病的发展

Dan Huang¹, Yamin Yuan¹, Liyuan Cao¹

¹Hongqiao International Institute of Medicine, Shanghai Tongren Hospital, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Faculty of Basic Medicine, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China.

Cellular oncology (Dordrecht, Netherlands)

|September 26, 2023

概括

血管蛋白排序33b (VPS33B) 在内皮细胞中通过通过小细胞外囊 (SEV) 分泌血管蛋白类蛋白2 (ANGPTL2) 来促进白血病. 这种相互作用维持了B细胞淋巴细胞白血病 (B-ALL) 的进展.

科学领域:

血液学血液学血液学
细胞生物学细胞生物学
癌症研究癌症研究

背景情况:

骨髓对于白血病的发展至关重要.
利基成分影响白血病的机制尚未完全理解.

研究的目的:

研究内皮细胞 (EC) 衍生小细胞外囊泡 (SEVs) 在B细胞淋巴细胞白血病 (B-ALL) 中的作用.
阐明血管蛋白排序33b (VPS33B) 和骨髓利基中的血管蛋白类蛋白2 (ANGPTL2) 对B-ALL发展的具体贡献.

主要方法:

使用Cre/LoxP技术在小鼠利基细胞中条件淘汰Vps33b和Angptl2.
通过N-Myc过度表达建立一个小鼠B-ALL模型.
流细胞测量用于白血病细胞和LIC检测.
SEV隔离,质谱,免疫沉和西部斑点来分析SEV和蛋白质相互作用.

主要成果:

在EC中对Vps33b的特定淘汰减少了SEV分泌,并延迟了B-ALL的进展.
Vps33b knockdown ECs 分泌的含有 ANGPTL2 的 SEV 较少.
在EC中Angptl2的有条件淘汰显著延迟了B-ALL的进展.
VPS33B与ANGPTL2直接相互作用; ANGPTL2中的突变降低了SEV分泌和白血病产生潜力.

结论:

由内皮细胞衍生的含有ANGPTL2的SEV维持B-ALL细胞活动.
VPS33B和ANGPTL2之间的相互作用调节了ANGPTL2-SEV的分泌.
利基特定的SEV在B-ALL发展中发挥着至关重要的作用.

关键词:

ANGPTL2 的角度.在B-ALL发展方面.内皮细胞是内皮细胞.在SEVs中,SEVs是SEV.这就是VPS33B.

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