Acyltransferase activity and cytochemical localization in differentiating neuroblastoma.
Acyltransferase (AT) enzyme activity was assayed biochemically and localized cytochemically in neuroblastoma monolayers to investigate the possible role of the enzyme in neuroblastoma differentiation and neurite extension. Treatment of cultures for 1 day with serum-free medium or Ro20-1724, a cyclic AMP phosphodiesterase inhibitor, induced neurite outgrowth but did not alter acyltransferase activity. Treatment for 4 days with dexamethasone or Ro20-1724 induced neurite outgrowth and a doubling of enzyme activity per cell. Chromatographic separation of lipid classes indicated that dexamethasone enhanced triacylglyceride synthesis. Acyltransferase was localized in mitochondria of neuroblastoma cells. The results show that 1) dexamethasone stimulates the storage lipid metabolic pathway in neuroblastoma cells and 2) increased acyltransferase activity is concomitant with dexamethasone-induced morphological differentiation. However, AT activity and neurite extension may not be causally related.
D051103:1-Acylglycerol-3-Phosphate O-Acyltransferase; D012368:4-(3-Butoxy-4-methoxybenzyl)-2-imidazolidinone / Q000494:pharmacology; D000217:Acyltransferases / Q000378:metabolism*; D002454:Cell Differentiation; D002460:Cell Line; D003907:Dexamethasone / Q000494:pharmacology; D050356:Lipid Metabolism; D008928:Mitochondria / Q000201:enzymology; D009447:Neuroblastoma / Q000201:enzymology* / Q000648:ultrastructure
D012368:4-(3-Butoxy-4-methoxybenzyl)-2-imidazolidinone; D003907:Dexamethasone; D000217:Acyltransferases; D051103:1-Acylglycerol-3-Phosphate O-Acyltransferase