Involvement of PGE2 and PGDH but not COX-2 in thrombin-induced cortical neuron apoptosis.
Neurosci Lett
; 452(2): 172-5, 2009 Mar 13.
Article
en En
| MEDLINE
| ID: mdl-19383433
ABSTRACT
The pathways that contribute to thrombin-induced neuron death have been incompletely defined. Induction of cyclooxygenase 2 (COX-2), the enzyme that catalyzes the first step in prostaglandin synthesis, promotes neuronal injury. PGE2, a downstream product of COX-2 metabolism, is neurotoxic in vitro and in vivo, and is thought to be the bioactive mediator responsible for COX-2 neurotoxicity. The objective of this study is to determine the ability of thrombin to affect PGE2 metabolism in cultured neurons. The data show that in thrombin-induced apoptosis of cultured neurons, PGE2 release increases when COX-2 is absent, and is regulated by prostaglandin dehydrogenase (PGDH), a key enzyme that degrades PGE2. NS398, a COX-2 specific inhibitor, protects neurons against thrombin toxicity, by inducing active PGDH. These data implicate PGDH in thrombin-mediated neuronal cell death.
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Trombina
/
Dinoprostona
/
Hidroxiprostaglandina Deshidrogenasas
/
Apoptosis
/
Ciclooxigenasa 2
/
Degeneración Nerviosa
Límite:
Animals
Idioma:
En
Revista:
Neurosci Lett
Año:
2009
Tipo del documento:
Article
País de afiliación:
Estados Unidos