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Blood, Vol. 92 No. 8 (October 15), 1998:
pp. 2759-2765
Lipopolysaccharide Induces the Antiapoptotic Molecules, A1 and
A20, in Microvascular Endothelial Cells
Xiaolong Hu,
Esther Yee,
John M. Harlan,
Fred Wong, and
Aly Karsan
From the Department of Pathology and Laboratory Medicine, University
of British Columbia and St Paul's Hospital, Vancouver, British
Columbia, Canada; and the Division of Hematology, University of
Washington, Seattle, WA.
The effect of lipopolysaccharide (LPS) on endothelial cells is a key
component of the inflammatory response seen in Gram-negative sepsis.
LPS does not cause death of cultured human endothelial cells. However,
when the expression of new proteins is inhibited by cycloheximide,
microvascular endothelial cells in culture undergo apoptosis. This
finding suggests that LPS induces apoptotic and antiapoptotic pathways,
with the antiapoptotic response being dependent on the synthesis of new
proteins. Concurrent activation of apoptotic and antiapoptotic pathways
has previously been documented for tumor necrosis factor (TNF). In the
case of TNF, the antiapoptotic signal has been attributed to at least
two cytoprotective proteins: the Bcl-2 homologue, A1, and the
zinc-finger protein, A20. In this study, we demonstrate that both these
molecules are induced in microvascular endothelial cells by LPS.
Enforced overexpression of either A1 or A20 inhibits LPS and
cycloheximide-initiated apoptosis. Induction of A1 and A20 does not
require synthesis of intermediary proteins, but is dependent on the
presence of soluble CD14. In addition, we show that inhibition of
signaling by the transcription factor, NF- B, blocks accumulation of
A1 and A20 mRNA. Taken together, our findings suggest that LPS directly
induces expression of the cytoprotective proteins, A1 and A20, via a
CD14-dependent pathway requiring activation of NF-B.
© 1998 by The American Society of Hematology.
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