生物
祖细胞
SMAD公司
细胞生物学
干细胞
造血
骨形态发生蛋白
造血干细胞
骨髓
信号转导
免疫学
遗传学
基因
作者
Jonas Larsson,Stefán Karlsson
出处
期刊:Oncogene
[Springer Nature]
日期:2005-08-29
卷期号:24 (37): 5676-5692
被引量:171
标识
DOI:10.1038/sj.onc.1208920
摘要
The TGF-beta family of ligands, including TGF-beta, bone morphogenetic protein (BMP) and activin, signal through Smad pathways to regulate the fate of hematopoietic progenitor and stem cells during development and postnatally. BMP regulates hematopoietic stem cell (HSC) specification during development, while TGF-beta1, 2 and 3 are not essential for the generation of HSCs. BMP4 can increase proliferation of human hematopoietic progenitors, while TGF-beta acts as a negative regulator of hematopoietic progenitor and stem cells in vitro. In contrast, TGF-beta signaling deficiency in vivo does not affect proliferation of HSCs and does not affect lineage choice either. Therefore, the outcome of Smad signaling is very context dependent in hematopoiesis and regulation of hematopoietic stem and progenitor cells is more complicated in the bone marrow microenvironment in vivo than is seen in liquid cultures ex vivo. Smad signaling regulates hematopoiesis by crosstalk with other regulatory signals and future research will define in more detail how the various pathways interact and how the knowledge obtained can be used to develop advanced cell therapies.
科研通智能强力驱动
Strongly Powered by AbleSci AI