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B Activity in Hemopoietic Progenitor Cells1
,,
*
H. Lee Moffitt Cancer Center, University of South Florida, Tampa, FL 33612;
Cardinal Bernardin Cancer Center and Departments of
Microbiology and Immunology and
Pathology, Loyola University Medical Center, Maywood, IL 60153; and
¶ Department of Veterinary and Animal Sciences, University of Massachusetts, Amherst, MA, 01003
We investigated the interaction between two elements critical for
differentiation of hemopoietic cells, the Notch-1 receptor and the
transcription factor NF-
B. These factors were studied in hemopoietic
progenitor cells (HPC) using Notch-1 antisense transgenic (Notch-AS-Tg)
mice. DNA binding of NF-B as well as its ability to activate
transcription was strongly decreased in HPC from Notch-AS-Tg mice.
NF-B-driven transcriptional activity was completely restored after
transduction of the cells with retroviral constructs containing
activated Notch-1 gene. HPC from Notch-AS-Tg mice have decreased levels
of several members of the NF-B family, p65, p50, RelB, and c-Rel and
this is due to down-regulation of the gene expression. To investigate
functional consequences of decreased NF-B activity in transgenic
mice, we studied LPS-induced proliferation of B cells and
GM-CSF-dependent differentiation of dendritic cells from HPC. These two
processes are known to be closely dependent on NF-B. B cells from
Notch-AS-Tg mice had almost 3-fold lower response to LPS than B cells
isolated from control mice. Differentiation of dendritic cells was
significantly affected in Notch-AS-Tg mice. However, it was restored by
transduction of activated Notch-1 into HPC. Taken together, these data
indicate that in HPC NF-B activity is regulated by Notch-1 via
transcriptional control of NF-B.
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