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1 alpha,25-dihydroxyvitamin D3-induced upregulation of calcineurin during
leukemic HL-60 cell differentiation
SB Omay, K Nakai, T Kuno, H Shiku and M Nishikawa
2nd Department of Internal Medicine, Mie University School of Medicine,
Tsu, Mie, Japan.
Cyclosporin A and FK506, at concentrations that inhibited phosphatase
activity of calcineurin in HL-60 cellular lysates, augmented the
proliferation of leukemic HL-60 cells. These immunosuppressants did not
affect 1 alpha,25-dihydroxyvitamin D3 [1,25(OH)2D3]-induced monocytic
differentiation of HL-60 cells, but did abrogate the 1,25(OH)2D3- induced
inhibition of HL-60 cell growth. Treatment with 20 nmol/L 1,25(OH)2D3 led
to a progressive increase in calcineurin phosphatase activity in
subcellular fractions from HL-60 cell extracts, the increase in this
activity appeared to parallel the phenotypic and functional changes of
HL-60 cells during monocytic differentiation induced by 1,25(OH)2D3.
Immunoblot analysis indicated that increase in calcineurin activity was
concordant with the increased expressions of calcineurin catalytic subunit
isozymes, calcineurin A alpha (CNA alpha), and calcineurin A beta(CNA
beta), and a regulatory calcineurin B subunit (CNB) proteins, which were
preceded by a coordinate increase in the levels of CNA alpha, CNA beta and
CNB mRNAs. The expression of calmodulin remained unaltered throughout
1,25(OH)2D3-induced monocytic differentiation. These results suggest that
calcineurin activation has a net negative effect on HL-60 cell
proliferation, and that the increased expression of calcineurin may be
involved in 1,25(OH)2D3- induced inhibition of HL-60 cell proliferation.
Volume 87,
Issue 7,
pp. 2947-2955,
04/01/1996
Copyright © 1996 by The American Society of Hematology
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