Abstract：
:To understand the role of FoxO family members in hematopoiesis, we conditionally deleted FoxO1, FoxO3, and FoxO4 in the adult hematopoietic system. FoxO-deficient mice exhibited myeloid lineage expansion, lymphoid developmental abnormalities, and a marked decrease of the lineage-negative Sca-1+, c-Kit+ (LSK) compartment that contains the short- and long-term hematopoietic stem cell (HSC) populations. FoxO-deficient bone marrow had defective long-term repopulating activity that correlated with increased cell cycling and apoptosis of HSC. Notably, there was a marked context-dependent increase in reactive oxygen species (ROS) in FoxO-deficient HSC compared with wild-type HSC that correlated with changes in expression of genes that regulate ROS. Furthermore, in vivo treatment with the antioxidative agent N-acetyl-L-cysteine resulted in reversion of the FoxO-deficient HSC phenotype. Thus, FoxO proteins play essential roles in the response to physiologic oxidative stress and thereby mediate quiescence and enhanced survival in the HSC compartment, a function that is required for its long-term regenerative potential.
journal_name
Celljournal_title
Cellauthors
Tothova Z,Kollipara R,Huntly BJ,Lee BH,Castrillon DH,Cullen DE,McDowell EP,Lazo-Kallanian S,Williams IR,Sears C,Armstrong SA,Passegué E,DePinho RA,Gilliland DGdoi
10.1016/j.cell.2007.01.003subject
Has Abstractpub_date
2007-01-26 00:00:00pages
325-39issue
2eissn
0092-8674issn
1097-4172pii
S0092-8674(07)00050-5journal_volume
128pub_type
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