期刊
BLOOD
卷 99, 期 1, 页码 95-101出版社
AMER SOC HEMATOLOGY
DOI: 10.1182/blood.V99.1.95
关键词
-
类别
资金
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [R01GM054351] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF MENTAL HEALTH [P30MH059037] Funding Source: NIH RePORTER
- NIAID NIH HHS [AI07334] Funding Source: Medline
- NIGMS NIH HHS [GM54351] Funding Source: Medline
- NIMH NIH HHS [P30 MH59037] Funding Source: Medline
The transcription factor signal transducers and activators of transcription 5 (STAT5) is activated by numerous cytokines that orchestrate blood cell development. Multilineage peripheral blood cytopenias were observed in adult mice lacking both isoforms of STAT5 (STAT5A and STAT5B) as well as accelerated rates of apoptosis in the bone marrow. Although the hematopoietic stem cell (HSC) population was preserved in a number of these mice, the post-HSC progenitor populations were: diminished and a marked reduction in functional progenitors (spleen colony-forming units) was detected. Competitive bone marrow transplantation studies in vivo revealed a profound impairment of repopulation potential of STAT5-null HSCs, leading to complete lack of contribution to the myeloid, erythroid, and lymphoid lineages. These abnormalities were associated with heightened proliferation activity in the HSC fraction, suggesting the action of homeostatic mechanisms to maintain sufficient levels of diverse blood cell types for viability. Thus, STAT5 normally sustains the robust hematopoietic reserve that contributes to host viability through crucial survival effects on early progenitor cells.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据