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Putative involvement of protein kinase C in proliferation of human myeloid
progenitor cells
N Katayama, M Nishikawa, N Minami and S Shirakawa
Second Department of Internal Medicine, Mie University School of Medicine,
Japan.
The effects of two different potent inhibitors of protein kinase C, 1-
(5-isoquinolinylsulfonyl)-2-methylpiperazine (H-7) and staurosporine on
human myeloid (CFU-C) and late erythroid progenitor cells (CFU-E) were
studied using an in vitro clonal assay. Our objective was to determine
whether protein kinase C has a role in signal transduction related to
proliferation of these committed progenitor cells. The presence of H-7 or
staurosporine led to an inhibition of colony formation stimulated by crude
colony-stimulating factor (CSF), interleukin-3 (IL-3),
granulocyte-macrophage CSF (GM-CSF), granulocyte CSF (G-CSF), or macrophage
CSF (M-CSF) in a dose-dependent manner. N-(2-guanidinoethyl)-
5-isoquinolinesulfonamide (HA-1004), a weaker analog of H-7, did not
inhibit proliferation of CFU-C. Neither H-7 nor staurosporine had any
effect on CFU-E formation. H-7 and staurosporine dose-dependently inhibited
the protein kinase C from K562 cells. The potential of these compounds to
inhibit proliferation of CFU-C correlated well with the magnitude of their
inhibition of protein kinase C from K562 cells. The inhibition of
proliferation of CFU-C appears to relate to the potential of these
compounds to inhibit protein kinase C. Thus, activation of protein kinase C
is presumably involved in the proliferation of CFU-C, and the regulatory
system of CFU-E appears to differ from that of CFU-C.
Volume 73,
Issue 1,
pp. 123-130,
01/01/1989
Copyright © 1989 by The American Society of Hematology
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