Role of protein kinases on NF- kappaB activation and cell death in bovine cerebral endothelial cells.
- Author:
Young Soo AHN
1
;
Chul Hoon KIM
;
Joo Hee KIM
Author Information
1. Department of Pharmacology, Yonsei University College of Medicine, Seoul, 120-752 South Korea.
- Publication Type:Original Article
- Keywords:
NF- kappaB;
Cerebral endothelial cell death;
Protein kinase
- MeSH:
Cell Death*;
Cell Survival;
Cyclic AMP-Dependent Protein Kinases;
Endothelial Cells*;
Protein Kinase C;
Protein Kinases*;
Protein-Tyrosine Kinases
- From:The Korean Journal of Physiology and Pharmacology
1999;3(1):11-18
- CountryRepublic of Korea
- Language:English
-
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.
