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Blood, 15 July 2001, Vol. 98, No. 2, pp. 303-312
HEMATOPOIESIS
Correlation between nicotine-induced inhibition of hematopoiesis
and decreased CD44 expression on bone marrow stromal cells
Sophia Khaldoyanidi,
Lyudmila Sikora,
Irina Orlovskaya,
Vera Matrosova,
Vladimir Kozlov, and
P. Sriramarao
From the Division of Vascular Biology, La Jolla
Institute for Molecular Medicine, La Jolla, CA; Institute for Clinical
Immunology, Novosibirsk, Russia; and the National Cancer
Institute-Frederick Cancer Research and Development Center, Frederick,
MD.
This study demonstrates that in vivo exposure to cigarette smoke
(CS) and in vitro treatment of long-term bone marrow cultures (LTBMCs)
with nicotine, a major constituent of CS, result in inhibition of
hematopoiesis. Nicotine treatment significantly delayed the onset of
hematopoietic foci and reduced their size. Furthermore, the number of
long-term culture-initiating cells (LTC-ICs) within an adherent layer
of LTBMCs was significantly reduced in cultures treated with nicotine.
Although the production of nonadherent mature cells and their
progenitors in nicotine-treated LTBMCs was inhibited, this treatment
failed to influence the proliferation of committed hematopoietic
progenitors when added into methylcellulose cultures. Bone marrow
stromal cells are an integral component of the hematopoietic
microenvironment and play a critical role in the regulation of
hematopoietic stem cell proliferation and self-renewal. Exposure to
nicotine decreased CD44 surface expression on primary bone
marrow-derived fibroblastlike stromal cells and MS-5 stromal cell
line, but not on hematopoietic cells. In addition, mainstream CS
altered the trafficking of hematopoietic stem/progenitor cells
(HSPC) in vivo. Exposure of mice to CS resulted in the
inhibition of HSPC homing into bone marrow. Nicotine and cotinine
treatment resulted in reduction of CD44 surface expression on
lung microvascular endothelial cell line (LEISVO) and bone
marrow-derived (STR-12) endothelial cell line. Nicotine treatment
increased E-selectin expression on LEISVO cells, but not on STR-12
cells. These findings demonstrate that nicotine can modulate
hematopoiesis by affecting the functions of the
hematopoiesis-supportive stromal microenvironment, resulting in the
inhibition of bone marrow seeding by LTC-ICs and interfering with stem
cell homing by targeting microvascular endothelial cells.
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