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

Authors
Seok, SM; Park, DH; Kim, YC; Moon, CH; Jung, YS; Baik, EJ; Moon, CK; Lee, SH
Citation
Toxicology letters, 165(3):212-220, 2006
Journal Title
Toxicology letters
ISSN
0378-42741879-3169
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.
MeSH terms
AnimalsBrain/blood supplyCadmium/toxicity*Cell Adhesion/physiologyCyclooxygenase 2/metabolism*Dinoprostone/metabolismDose-Response Relationship, DrugEndothelial Cells/drug effects*Endothelial Cells/metabolism*Gene Expression RegulationIntercellular Adhesion Molecule-1/metabolism*Leukocytes/metabolismMiceUp-Regulationp38 Mitogen-Activated Protein Kinases/metabolism
DOI
10.1016/j.toxlet.2006.04.007
PMID
16777358
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Physiology
AJOU Authors
문, 창현정, 이숙백, 은주이, 수환
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