细胞生物学
间充质干细胞
线粒体
串扰
骨重建
细胞命运测定
干细胞
细胞
生物
化学
生物化学
转录因子
内分泌学
基因
光学
物理
作者
Wenjin Cai,Jinglun Zhang,Yiqian Yu,Yueqi Ni,Wei Yan,Yihong Cheng,Litian Han,Leyi Xiao,Xiaoxin Ma,Hongjiang Wei,Yaoting Ji,Yufeng Zhang
标识
DOI:10.1002/advs.202204871
摘要
Mitochondria are the powerhouse of eukaryotic cells, which regulate cell metabolism and differentiation. Recently, mitochondrial transfer between cells has been shown to direct recipient cell fate. However, it is unclear whether mitochondria can translocate to stem cells and whether this transfer alters stem cell fate. Here, mesenchymal stem cell (MSC) regulation is examined by macrophages in the bone marrow environment. It is found that macrophages promote osteogenic differentiation of MSCs by delivering mitochondria to MSCs. However, under osteoporotic conditions, macrophages with altered phenotypes, and metabolic statuses release oxidatively damaged mitochondria. Increased mitochondrial transfer of M1-like macrophages to MSCs triggers a reactive oxygen species burst, which leads to metabolic remodeling. It is showed that abnormal metabolism in MSCs is caused by the abnormal succinate accumulation, which is a key factor in abnormal osteogenic differentiation. These results reveal that mitochondrial transfer from macrophages to MSCs allows metabolic crosstalk to regulate bone homeostasis. This mechanism identifies a potential target for the treatment of osteoporosis.
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