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In vitro biosynthesis of leukemia inhibitory factor/human interleukin for
DA cells by human endothelial cells: differential regulation by
interleukin-1 alpha and glucocorticoids
C Grosset, B Jazwiec, JL Taupin, H Liu, S Richard, FX Mahon, J Reiffers, JF Moreau and J Ripoche
Laboratoire de Greffe de Moelle, Universite de Bordeaux II, France.
Endothelial cell (EC) may represent a major source of cytokines in the bone
marrow. In this study we have examined the production and the regulation of
the production of leukemia inhibitory factor/human interleukin for DA cells
(LIF/HILDA) by EC. Human umbilical vein endothelial cells (HUVEC) were
chosen as a working model as they are a well known source of cytokines.
These cells secrete LIF/HILDA (90 pg/mL/10(6) cells/48 h) in basal
conditions. This secretion is profoundly altered by interleukin-1 alpha
(IL-1 alpha). Secretion of LIF/HILDA is increased threefold on stimulation
with IL-1 alpha at a concentration of 100 IU/mL. The secreted protein is
bioactive as demonstrated by its proliferative effects on DA1a cells.
Modulation of the production of LIF/HILDA by glucocorticoids (GC) was also
examined. In striking contrast to what was observed for IL-1 alpha, the
synthetic GC dexamethasone (DXM) at a concentration of 10(-6) mol/L
consistently inhibited the basal secretion of LIF/HILDA by an average of
threefold and suppressed the IL-1 alpha-induced increase of the secretion
of this cytokine by HUVEC. In an effort to extend results obtained with
HUVEC to the bone marrow endothelium, we have also examined the production
of LIF/HILDA by human bone marrow endothelial cells (HBMEC). Our study
shows that HBMEC are quantitatively a very important source of this
cytokine (above 7.25 ng/mL/10(6) cells/48 h) suggesting that they are a
major source of LIF/HILDA in the bone marrow. Again, IL-1 alpha proved to
be a very potent stimulus for the secretion of LIF/HILDA and synthetic GC
such as DXM when used at a concentration of 10(-6) mol/L inhibited by an
average of threefold the basal secretion of LIF/HILDA and had suppressive
effect on the IL-1 alpha-induced increase of this secretion. The
downregulation of LIF/HILDA production in the bone marrow by GC may be
important to understand the effects of GC on hematopoiesis.
Volume 86,
Issue 10,
pp. 3763-3770,
11/15/1995
Copyright © 1995 by The American Society of Hematology
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