Tumour necrosis factor (cachectin) induces phospholipase A2 activity and synthesis of a phospholipase A2-activating protein in endothelial cells

摘要: Tumour necrosis factor (TNF) is an important mediator of endotoxin-induced vascular collapse and other inflammatory reactions. Eicosanoids have been implicated in the pathogeensis these responses. In order to explore further potential interactions between TNF eicosanoid metabolism eliciting responses, we studied effects on bovine endothelial cell line CPAE. induced cellular retraction observed by light microscope. This morphological change was monitored passage iodinated protein A adjacent cells release [3H]arachidonic acid metabolites from cells. Both functional responses were abrogated inhibition synthesis with BW755c. The appeared be mediated a transient increase phospholipase A2 activity. Phospholipase C activity not affected TNF. maximal occurred at 5 min following addition activation, acid-metabolite A, required both RNA associated recently described A2-activating protein. Bordetella pertussis toxin, islet-activating protein, also inhibited activity, suggesting that receptor-ligand interaction resulting retraction, activation synthesis, coupled through Ni guanine nucleotide regulatory