COX-2 is associated with cadmium-induced ICAM-1 expression in cerebrovascular endothelial cells.
Toxicol Lett
; 165(3): 212-20, 2006 Sep 10.
Article
em En
| MEDLINE
| ID: mdl-16777358
ABSTRACT
In order to get insight into the mechanism of cadmium (Cd)-induced brain injury, we investigated the effects of Cd on the induction of COX-2 and ICAM-1 in bEnd.3 mouse brain endothelial cells (EC). Cd stimulated PGE(2) release in a time and dose dependent manner, which was accompanied by increase of COX-2 expression. The thiol-reducing antioxidant N-acetylcyteine attenuated Cd-induced PGE(2) production and COX-2 expression. Cd increased phosphorylation of p38 MAPK, but not of JNK and ERK1/2. A blockade of p38 MAPK pathway abrogated Cd-induced COX-2 expression and PGE(2) production. Cd-induced ICAM-1 expression and leukocyte-EC adhesion were diminished by non-steroidal anti-inflammatory drugs such as indomethacin and NS-398, which was reversed by addition of PGE(2). Together, these data suggest that Cd induces COX-2 expression through the activation of p38 MAPK, an oxidative stress-sensitive cellular signaling molecule, and induction of COX-2 is associated with ICAM-1 expression in brain endothelial cells following Cd exposure.
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Base de dados:
MEDLINE
Assunto principal:
Cádmio
/
Molécula 1 de Adesão Intercelular
/
Células Endoteliais
/
Ciclo-Oxigenase 2
Tipo de estudo:
Risk_factors_studies
Limite:
Animals
Idioma:
En
Revista:
Toxicol Lett
Ano de publicação:
2006
Tipo de documento:
Article
País de afiliação:
Coréia do Sul