Phosphatidate accumulation in hormone-treated hepatocytes via a phospholipase D mechanism.

摘要: Isolated rat hepatocytes responded to a variety of Ca2+-mobilizing agents (vasopressin, angiotensin II, epinephrine, epidermal growth factor, ATP, and ADP) with rapid increase in phosphatidate mass, as measured by sensitive new method. When were incubated vasopressin (10(-8) M), levels increased 2-3-fold 2 min, but there was no significant diacylglycerol at this time. Changes the fatty acid composition also preceded those diacylglycerol. De novo synthesis from [3H]glycerol unaffected short-term incubation. Incubation washed liver plasma membranes GTP gamma S caused time-dependent phosphatidate. [gamma-32P]ATP, incorporation 32P into observed. This excludes phospholipase C-diacylglycerol kinase pathway suggests that D activity produced At submaximal concentrations S, ATP ADP stimulated membrane formation, presumably acting through P2-purinergic receptors. Only phosphatidylcholine, among major phospholipids, decreased response S. The phosphatidylcholine may be source hormonally elicited We conclude hormones mainly mechanism does not involve phosphorylation or de involves guanine nucleotide-binding protein coupled D.