Journal
CELL STEM CELL
Volume 4, Issue 2, Pages 170-179Publisher
CELL PRESS
DOI: 10.1016/j.stem.2008.10.005
Keywords
-
Categories
Funding
- Howard Hughes Medical Institute
- U.S. Army Research Office [DAAD19-03-1-0168]
- University of Michigan (UM) Cancer Biology
- UM-Comprehensive Cancer
- NIH [CA46592]
- Rheumatic Core Disease Center [P30 AR48310]
Ask authors/readers for more resources
According to the osteoblastic niche model, hematopoietic stem cells (HSCs) are maintained by N-cadherin-mediated homophilic adhesion to osteoblasts at the bone marrow endosteum. In contrast to this model, we cannot detect N-cadherin expression by HSCs, and most HSCs do not localize to the endosteal surface. It has nonetheless been suggested that HSCs express low levels of N-cadherin that regulate HSC maintenance. To test this, we conditionally deleted N-cadherin from HSCs and other hernatopoietic cells in adult Mx-1-Cre(+)N-cadherin(fl/-) mice. N-cadherin deficiency had no detectable effect on HSC maintenance or hematopoiesis. N-cadherin deficiency did not affect bone marrow cellularity or lineage composition, the numbers of colony-forming progenitors, the frequency of HSCs, the ability of HSCs to sustain hematopoiesis over time, or their ability to reconstitute irradiated mice in primary or secondary transplants. Loss of N-cadherin does not lead to HSC depletion. N-cadherin expression by HSCs is not necessary for niche function.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available