Andro treatment and p50 knock-out inhibit TF activity and
expression in stimulated human and murine endothelial cells and
monocytes/macrophages. A–D, HUVECs (A), human
adherent macrophages (B), C57BL/6J PVECs (C), and C57BL/6J
macrophages (D) were stimulated with LPS, TNF-α, and PMA, in
the presence of buffer (-), DMSO (a solvent control), 4H-Andro (an inactive
structural analog), and Andro. Cell lysates were measured for TF activity
(upper panels) and TF expression (lower panels). Results are
presented as either the mean ± S.D. value of triplicate measurements of
three independent experiments (upper panels,*, p
< 0.05; **, p < 0.01 versus DMSO group) or
a representative of three independent experiments (lower panels).
Although 4H-Andro appeared to partially inhibit TF activity and mRNA induced
by TNF-α and PMA, these differences were not statistically significant
(p > 0.05). E and F, TF activity and expression
in stimulated endothelial cells and macrophages isolated from p50
null mice. PVECs (E) and macrophages (F) were isolated from
B6 mice and p50 null mice. Following treatment with LPS, TNF-α,
and PMA in the absence or presence of 4H-Andro and Andro, the activity
(upper panels) and expression (lower panels) of TF were
measured. Results are presented as either the mean ± S.D. value of
triplicate measurements of three independent experiments (upper
panels,*, p < 0.05; **, p <
0.01 versus B6 group) or a representative of three independent
experiments (lower panels).