作者: S. Oka , H. Arita
DOI: 10.1016/S0021-9258(18)92912-1
关键词: Biology 、 Protein kinase A 、 Cell biology 、 Gene expression 、 Protein kinase C 、 Activator (genetics) 、 Internal medicine 、 Tumor necrosis factor alpha 、 Endocrinology 、 Regulation of gene expression 、 Kinase 、 Phospholipase A2
摘要: Inflammatory factors such as tumor necrosis factor (TNF), interleukin 1 (IL-1), and lipopolysaccharide (LPS) greatly enhance the expression of group II phospholipase A2 (PLA2-II) mRNA, leading to increased secretion PLA2-II enzyme from rat-cultured astrocytes. The potent antiinflammatory agent dexamethasone suppressed induced by LPS. In vivo studies also demonstrated that level mRNA in brain with intravenous injection These results suggest plays important roles inflammatory response. Agents which increase intracellular cAMP concentration did not stimulate themselves but selectively enhanced TNF-induced about 5-fold. Phorbol ester, a well known protein kinase C activator, expression. H-7, inhibitor, inhibited LPS-induced expression, inhibit one. Therefore, we conclude TNF-activated pathway differs LPS-activated one: former is latter involves C.