z-logo
open-access-imgOpen Access
Stimulation with thromboxane A 2 (TXA 2 ) receptor agonist enhances ICAM‐1, VCAM‐1 or ELAM‐1 expression by human vascular endothelial cells
Author(s) -
Toshiaki Ishizuka,
Makoto Kawakami,
Toshihiko Hidaka,
Yasunori Matsuki,
Mitsuyo Takamizawa,
Kunihiro Suzuki,
Akira Kurita,
Haruo Nakamura
Publication year - 1998
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1046/j.1365-2249.1998.00614.x
Subject(s) - thromboxane a2 , intercellular adhesion molecule 1 , receptor , cell adhesion molecule , vcam 1 , agonist , biology , microbiology and biotechnology , protein kinase c , icam 1 , signal transduction , biochemistry
A previous study reported that intercellular adhesion molecule‐1 (ICAM‐1) expression by human vascular endothelial cells (HUVEC) is augmented by intracellular signal transmission mainly through the protein kinase C (PKC) system stimulated by TXA 2 receptors. In the present study, we show that a TXA 2 receptor agonist, U46619, augments the expression of not only ICAM‐1, but also vascular cell adhesion molecule‐1 (VCAM‐1) or endothelial leucocyte adhesion molecule‐1 (ELAM‐1) in HUVEC both at protein and mRNA levels. Pretreatment with SQ29,548 (a TXA 2 receptor antagonist) or PKC inhibitors greatly diminished the extent of U46619‐induced mRNA accumulation and surface expression of the adhesion molecules. An inhibitor of nuclear factor κB (NF‐κB) activation, PDTC, diminishes U46619‐induced VCAM‐1 mRNA accumulation. NAC, which inhibits NF‐κB and activation protein 1 (AP‐1) binding activity, inhibits the expression of ICAM‐1 or ELAM‐1 at protein and mRNA levels. These findings suggest that ICAM‐1 or ELAM‐1 expression of HUVEC stimulated via TXA 2 receptors is augmented by induction of NF‐κB and AP‐1 binding activity through the PKC system, and that VCAM‐1 expression is augmented by induction of NF‐κB binding activity.

The content you want is available to Zendy users.

Already have an account? Click here to sign in.
Having issues? You can contact us here