Role of protein kinases on NF- kappaB activation and cell death in bovine cerebral endothelial cells
The Korean Journal of Physiology and Pharmacology
;
: 11-18, 1999.
Artículo
en Inglés
| WPRIM
| ID: wpr-728038
ABSTRACT
Nuclear factor kappaB (NF- kappaB) activation is modulated by various protein kinases. Activation of NF- kappaB is known to be important in the regulation of cell viability. The present study investigated the effect of inhibitors of protein tyrosine kinase (PTK), protein kinase C (PKC) and protein kinase A (PKA) on NF- kappaB activity and the viability of bovine cerebral endothelial cells (BCECs). In serum-deprivation-induced BCEC death, low doses of TNF alpha showed a protective effect. TNF alpha induced NF- kappaB activation within 4 h in serum-deprivation. PTK inhibitors (herbimycin A and genistein) and PKC inhibitor (calphostin C) prevented NF- kappaB activation stimulated by TNF alpha. Likewise, these inhibitors prevented the protective effect of TNF alpha. In contrast to TNF alpha-stimulated NF- kappaB activity, basal NF- kappaB activity of BCECs in media containing serum was suppressed only by calphostin C, but not by herbimycin A. As well BCEC death was also induced only by calphostin C in serum-condition. H 89, a PKA inhibitor, did not affect the basal and TNF alpha-stimulated NF- kappaB activities and the protective effect of TNF alpha on cell death. These data suggest that modulation of NF- kappaB activation could be a possible mechanism for regulating cell viability by protein kinases in BCECs.
Texto completo:
Disponible
Índice:
WPRIM (Pacífico Occidental)
Asunto principal:
Proteínas Quinasas
/
Proteína Quinasa C
/
Proteínas Tirosina Quinasas
/
Supervivencia Celular
/
Muerte Celular
/
Proteínas Quinasas Dependientes de AMP Cíclico
/
Células Endoteliales
Idioma:
Inglés
Revista:
The Korean Journal of Physiology and Pharmacology
Año:
1999
Tipo del documento:
Artículo
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