Lead induces COX-2 expression in glial cells in a NFAT-dependent, AP-1/NFκB-independent manner.
Toxicology
; 325: 67-73, 2014 Nov 05.
Article
en En
| MEDLINE
| ID: mdl-25193092
Epidemiologic studies have provided solid evidence for the neurotoxic effect of lead for decades of years. In view of the fact that children are more vulnerable to the neurotoxicity of lead, lead exposure has been an urgent public health concern. The modes of action of lead neurotoxic effects include disturbance of neurotransmitter storage and release, damage of mitochondria, as well as induction of apoptosis in neurons, cerebrovascular endothelial cells, astroglia and oligodendroglia. Our studies here, from a novel point of view, demonstrates that lead specifically caused induction of COX-2, a well known inflammatory mediator in neurons and glia cells. Furthermore, we revealed that COX-2 was induced by lead in a transcription-dependent manner, which relayed on transcription factor NFAT, rather than AP-1 and NFκB, in glial cells. Considering the important functions of COX-2 in mediation of inflammation reaction and oxidative stress, our studies here provide a mechanistic insight into the understanding of lead-associated inflammatory neurotoxicity effect via activation of pro-inflammatory NFAT3/COX-2 axis.
Palabras clave
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Neuroglía
/
FN-kappa B
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Factor de Transcripción AP-1
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Intoxicación del Sistema Nervioso por Plomo
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Ciclooxigenasa 2
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Factores de Transcripción NFATC
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Plomo
Límite:
Animals
Idioma:
En
Revista:
Toxicology
Año:
2014
Tipo del documento:
Article
País de afiliación:
Estados Unidos
Pais de publicación:
Irlanda