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Growth factor-dependent proliferative stimulation of hematopoietic cells is
associated with the modulation of cytoplasmic and nuclear 68- Kd
calmodulin-binding protein
GP Reddy, WC Reed, DH Deacon and PJ Quesenberry
Department of Obstetrics and Gynecology, University of Virginia Health
Sciences Center, Charlottesville 22908.
Calcium and calmodulin (CaM) are known to play critical roles in
controlling cell cycle progression in a variety of cells. We observed that
the CaM antagonist, N-(6-aminohexyl)-5-chloro-1- naphthalensulfonamide
hydrochloride (W-7), inhibited 3H-thymidine incorporation into DNA of
factor-dependent hematopoietic cells. To delineate the role of CaM in
proliferation of hematopoietic cells, we have investigated intracellular
distribution of specific CaM-binding proteins (CaM-BPs) in response to
hematopoietic growth factors in FDC- P1, 32D, NFS-60, and T1165 cells. Each
of these cell lines, when deprived of cytokines for 16 to 18 hours,
essentially ceased proliferation, even in the presence of fetal calf serum.
Concomitant to the cessation of proliferation, there was a dramatic
depletion of a specific CaM-BP of about 68 Kd in both their cytoplasmic and
nuclear fractions. Within 6 to 12 hours of reexposure to
proliferation-specific cytokines, there was a restoration of the nuclear as
well as cytoplasmic 68-Kd CaM-BP. Furthermore, such an induction and
nuclear localization of the 68-Kd CaM-BP by the cytokines coincided
temporally with the progression of synchronized FDC-P1 cells from G1 to S
phase. By contrast, colony-stimulating factor-1 (CSF-1)-dependent bone
marrow macrophages and BAC-1 cells did not exhibit 68-Kd CaM-BP in the
nuclear or cytoplasmic fractions. These studies suggest that while
hematopoietic growth factor granulocyte CSF-, granulocyte-macrophage CSF-,
interleukin-3 (IL-3)-, or IL-6-, whose receptors are members of the
hematopoietin receptor family, induced cell proliferation is associated
with a common mechanism involving nuclear localization of the 68-Kd CaM-BP,
the CSF-1-induced proliferation seems to involve 68- Kd CaM-BP-independent
pathways.
Volume 79,
Issue 8,
pp. 1946-1955,
04/15/1992
Copyright © 1992 by The American Society of Hematology
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