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A20 Inhibits NF- B Activation in Endothelial Cells Without
Sensitizing to Tumor Necrosis Factor-Mediated Apoptosis
Christiane Ferran,
Deborah M. Stroka,
Anne Z. Badrichani,
Jeffrey
T. Cooper,
Christopher J. Wrighton,
Miguel Soares,
Shane T. Grey, and
Fritz H. Bach
From the Department of Surgery, Center por Immunobiology, Beth Israel
Deaconess Medical Center, Harvard Medical School, Boston MA; and
Therexsys Ltd, The Science Park, Keele University, Keele,
Staffordshire, UK.
Expression of the NF- B-dependent gene A20 in endothelial cells
(EC) inhibits tumor necrosis factor (TNF)-mediated apoptosis in the
presence of cycloheximide and acts upstream of IB degradation to
block activation of NF-B. Although inhibition of NF-B by IB
renders cells susceptible to TNF-induced apoptosis, we show that when
A20 and IB are coexpressed, the effect of A20 predominates in
that EC are rescued from TNF-mediated apoptosis. These findings place
A20 in the category of "protective" genes that are induced in
response to inflammatory stimuli to protect EC from unfettered activation and from undergoing apoptosis even when NF-B is blocked. From a therapeutic perspective, genetic engineering of EC to express an
NF-B inhibitor such as A20 offers the mean of achieving an anti-inflammatory effect without sensitizing the cells to TNF-mediated apoptosis.
Blood, Vol. 91 No. 7 (April 1), 1998:
pp. 2249-2258
© 1998 by The American Society of Hematology.
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