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Calcium influx in induced differentiation of murine erythroleukemia cells
B Gillo, YS Ma and AR Marks
Department of Medicine, Brookdale Center for Molecular Biology, Mount Sinai
School of Medicine, New York, NY 10029.
Murine erythroleukemia cells (MELC) have served as a model for examining
the regulation of erythroid differentiation. However, the role of Ca2+ in
the signal transduction pathways regulating differentiation remains
unclear. To begin to address this uncertainty we have characterized the
regulation of cytoplasmic Ca2+ and the possible role of calcium channels
during induced differentiation in MELC. MELC can be induced to terminal
differentiation using the polar/apolar compound hexamethylene bisacetamide
(HMBA). We found that HMBA stimulated Ca2+ influx within 3 to 6 minutes and
that Ca2+ entry was required but not sufficient for MELC growth and
differentiation. Nifedipine (1 to 10 mumol/L), a calcium channel
antagonist, blocked HMBA-induced Ca2+ influx and inhibited differentiation
by approximately 60%. Depolarization of the MELC membrane did not induce
Ca2+ influx and whole-cell patch-clamp recordings failed to detect a
voltage-activated Ca2+ current, suggesting that MELC do not express
detectable levels of a functional voltage-dependent calcium channel (VDCC).
However, a cDNA probe encoding a portion of the alpha 1 subunit of the
cardiac VDCC detected an approximately 8-kb mRNA on Northern blots of total
MELC RNA. Taken together, these data show that Ca2+ influx is an early
event associated with HMBA-induced differentiation in MELC, blockade of
this calcium influx inhibits induced differentiation, and a voltage-
insensitive dihydropyridine-sensitive calcium channel may be involved in
Ca2+ influx in MELC.
Volume 81,
Issue 3,
pp. 783-792,
02/01/1993
Copyright © 1993 by The American Society of Hematology
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