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Studies on bioactive gangliosides: II. Requirement of ganglioside GD1a for prolonged GQ1b-driven nerve growth promotion in neuroblastoma cell lines.

Abstract
The novel effects of gangliosides from human brain on the number of nuclei of nerve cells and neurite outgrowth were studied in cultures of human neuroblastoma cell lines GOTO and NB-1. Ganglioside GQ1b at a nanomolar level stimulated cell proliferation and neurite outgrowth during culture for 24 hours, as reported previously [J Biochem 94: 303-306, 1983]. Although the neurite promoting activity of GQ1b was similar to those of total human brain gangliosides (GS) and nerve growth factor (NGF), its activity on cell proliferation did not persist on longer culture; that is, the number of GQ1b-treated cells rapidly decreased to the control level during culture for 48 or 72 hours. In contrast, on treatment with GS or NGF, the number of cell nuclei increased continuously during prolonged culture. These results showed that either some other molecular species of ganglioside(s) than GQ1b or other substances such as proteins present in the GS fraction were responsible for the long-term activity. Studies on the GS fraction after its treatment with proteases and neuraminidases revealed that ganglioside GD1a (20 ng/ml) had the ability to prolong the activity of GQ1b. Namely, GQ1b and GD1a gangliosides cooperated in maintaining the number of nuclei in long-term cultures of neuroblastoma cell lines.
AuthorsM Arita, S Tsuji, M Omatsu, Y Nagai
JournalJournal of neuroscience research (J Neurosci Res) Vol. 12 Issue 2-3 Pg. 289-97 ( 1984) ISSN: 0360-4012 [Print] United States
PMID6502754 (Publication Type: Comparative Study, Journal Article)
Chemical References
  • Gangliosides
  • Nerve Growth Factors
  • ganglioside, GD1a
  • GQ1b ganglioside
Topics
  • Cell Differentiation (drug effects)
  • Cell Division (drug effects)
  • Cell Line
  • Cell Nucleus (drug effects)
  • Gangliosides (isolation & purification, pharmacology)
  • Humans
  • Nerve Growth Factors
  • Neuroblastoma
  • Neurons (drug effects)

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