Insulin and insulin-like growth factor II permit nerve growth factor binding and the neurite formation response in cultured human neuroblastoma cells.
In serum-free medium, SH-SY5Y human neuroblastoma cells specifically and reversibly lost the capacity to bind 125I-labeled nerve growth factor (NGF) to the high-affinity sites (slow sites) and to respond by neurite outgrowth, unless physiological concentrations of insulin or insulin-like growth factor II were present. In serum-containing medium, anti-insulin antiserum decreased the neurite formation response to NGF, and insulin supplementation increased the number of available NGF slow sites. The low-affinity NGF fast sites are absent from SH-SY5Y cells and did not emerge on treatment with insulin. Insulin potentiated the induction of neurites by NGF in rat pheochromocytoma PC12 cells also. These results implicate a wider role for insulin and its homologs in the nervous system.
D000818:Animals; D001369:Axons / Q000187:drug effects / Q000502:physiology*; D002478:Cells, Cultured; D003470:Culture Media; D066246:ErbB Receptors; D006801:Humans; D007106:Immune Sera; D007328:Insulin / Q000494:pharmacology*; D007700:Kinetics; D009414:Nerve Growth Factors / Q000378:metabolism*; D009447:Neuroblastoma / Q000503:physiopathology*; D010455:Peptides / Q000494:pharmacology*; D051381:Rats; D011956:Receptors, Cell Surface / Q000378:metabolism*; D013002:Somatomedins / Q000494:pharmacology*
D003470:Culture Media; D007106:Immune Sera; D007328:Insulin; D009414:Nerve Growth Factors; D010455:Peptides; D011956:Receptors, Cell Surface; D013002:Somatomedins; D066246:ErbB Receptors