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Nitric oxide modulation of human leukemia cell differentiation and gene
expression
G Magrinat, SN Mason, PJ Shami and JB Weinberg
Division of Hematology-Oncology, VA Medical Center, Durham, NC.
Nitric oxide (NO) functions as an intercellular messenger molecule in such
varied contexts as neurotransmission, immune regulation, and the control of
vascular tone. We report that NO, delivered as purified gas or released
from the pharmacologic NO donors sodium nitroprusside or 6-
morpholino-sydnonimine, caused monocytic differentiation of cells of the
human myeloid leukemia cell line HL-60 and altered gene expression. The
treated cells stopped proliferating, became spread and vacuolated, had
increased expression of nonspecific esterase and the monocyte marker CD14,
and displayed increased capacity to produce hydrogen peroxide. Furthermore,
these treated cells had increased steady-state expression of messenger RNA
(mRNA) for tumor necrosis factor-alpha (TNF- alpha) and interleukin-1 beta
(IL-1 beta), but decreased expression of mRNA for the proto-oncogenes c-myc
and c-myb. The increase in TNF-alpha and IL-1 beta mRNA levels was due (at
least in part) to a new transcription of these specific mRNAs. NO
elaborated in the bone marrow microenvironment may have a role in normal
and malignant hematopoietic cell growth and differentiation.
Volume 80,
Issue 8,
pp. 1880-1884,
10/15/1992
Copyright © 1992 by The American Society of Hematology
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