COX-2 is associated with cadmium-induced ICAM-1 expression in cerebrovascular endothelial cells

Sun Mi Seok, Dong Hyun Park, Young Chae Kim, Chang Hyun Moon, Yi Sook Jung, Eun Joo Baik, Chang Kiu Moon, Soo Hwan Lee

Research output: Contribution to journalArticlepeer-review


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 PGE2 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 PGE2 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 PGE2 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 PGE2. 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.

Original languageEnglish (US)
Pages (from-to)212-220
Number of pages9
JournalToxicology Letters
Issue number3
StatePublished - Sep 10 2006
Externally publishedYes


  • Brain endothelial cells
  • Cadmium
  • Cyclooxygenase-2
  • ICAM-1

ASJC Scopus subject areas

  • Toxicology


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