Does phospholipid methylation play a role in the primary mechanism of action of nerve growth factor?
Nerve growth factor (NGF)-untreated (naive) and neurite-bearing NGF-treated ("primed") PC12 rat pheochromocytoma cells were used as model system to study the role of phospholipid methylation in the NGF mechanism of action. The neurite-bearing cultures were deprived of NGF for 3 h before experimentation. Under both experimental conditions, the cells were labelled with [methyl-3H]methionine and then challenged with NGF for time periods ranging from 5 s to 30 min. Methylated phospholipids were extracted and then resolved and identified by TLC as phosphatidyl mono-, di-, and trimethyl ethanolamine. Quantification of the amount of radioactivity incorporated into each of the phospholipids indicated that NGF does not significantly alter phospholipid methylation either in naive or in neurite-bearing cells. Furthermore, using a methyltransferase inhibitor, it was found that neurite outgrowth still occurs when phospholipid methylation is almost completely blocked. These results indicate that phospholipid methylation does not play a primary role in the mechanism of action of NGF.
D000818:Animals; D002460:Cell Line; D002855:Chromatography, Thin Layer; D008745:Methylation; D009414:Nerve Growth Factors / Q000494:pharmacology* / Q000502:physiology; D009474:Neurons / Q000187:drug effects / Q000254:growth & development; D010714:Phosphatidylethanolamines / Q000302:isolation & purification / Q000378:metabolism; D010743:Phospholipids / Q000378:metabolism / Q000502:physiology*; D051381:Rats
D009414:Nerve Growth Factors; D010714:Phosphatidylethanolamines; D010743:Phospholipids