生物
干细胞
造血
离体
骨髓
细胞生物学
CDC42型
淋巴细胞生成
造血干细胞
利基
免疫学
体内
信号转导
遗传学
生态学
作者
Novella Guidi,Gina Marka,Vadim Sakk,Yi Zheng,Maria Carolina Florian,Hartmut Geiger
出处
期刊:Stem Cells
[Wiley]
日期:2021-04-13
卷期号:39 (8): 1101-1106
被引量:9
摘要
Abstract Aging-associated leukemia and aging-associated immune remodeling are in part caused by aging of hematopoietic stem cells (HSCs). An increase in the activity of the small RhoGTPase cell division control protein 42 (Cdc42) within HSCs causes aging of HSCs. Old HSCs, treated ex vivo with a specific inhibitor of Cdc42 activity termed CASIN, stay rejuvenated upon transplantation into young recipients. We determined in this study the influence of an aged niche on the function of ex vivo rejuvenated old HSCs, as the relative contribution of HSCs intrinsic mechanisms vs extrinsic mechanisms (niche) for aging of HSCs still remain unknown. Our results show that an aged niche restrains the function of ex vivo rejuvenated HSCs, which is at least in part linked to a low level of the cytokine osteopontin found in aged niches. The data imply that sustainable rejuvenation of the function of aged HSCs in vivo will need to address the influence of an aged niche on rejuvenated HSCs.
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