Protein kinase A mediates microglial activation induced by plasminogen and gangliosides
Experimental & Molecular Medicine
;
: 461-467, 2004.
Article
Dans Anglais
| WPRIM
| ID: wpr-226075
ABSTRACT
In the injured brain, microglia is known to be activated and produce proinflammatory mediators such as interleukin-1beta (IL-1beta), tumor necrosis factor-alpha (TNF-alpha) and inducible nitric oxide synthase (iNOS). We investigated the role of protein kinase A (PKA) in microglial activation by both plasminogen and gangliosides in rat primary microglia and in the BV2 immortalized murine microglial cell line. Both plasminogen and gangliosides induced IL-1beta, TNF-alpha and iNOS mRNA expression, and that this expression was inhibited by the addition of the PKA inhibitors, KT5720 and H89. Both plasminogen and gangliosides activated PKA and increased the DNA binding activity of the cAMP response element- binding protein (CREB). Furthermore, KT5720 and H89 reduced the DNA binding activities of CREB and NF-kappaB in plasminogen-treated cells. These results suggest that PKA plays an important role in plasminogen and gangliosides- induced microglial activation.
Texte intégral:
Disponible
Indice:
WPRIM (Pacifique occidental)
Sujet Principal:
Plasminogène
/
Pyrroles
/
Sulfonamides
/
ARN messager
/
Carbazoles
/
Lignée cellulaire
/
Régulation de l'expression des gènes
/
Facteur de transcription NF-kappa B
/
Interleukine-1
/
Facteur de nécrose tumorale alpha
Limites du sujet:
Animaux
langue:
Anglais
Texte intégral:
Experimental & Molecular Medicine
Année:
2004
Type:
Article
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