FGF2 and dual agonist of NCAM and FGF receptor 1, Enreptin, rescue neurite outgrowth loss in hippocampal neurons expressing mutated huntingtin proteins

Mirolyuba Ilieva*, Troels T. Nielsen, Tanja Michel, Stanislava Pankratova

*Corresponding author for this work

Research output: Contribution to journalJournal articleResearchpeer-review

Abstract

In the present study, we developed an in vitro model of Huntington disease (HD) by transfecting primary rat hippocampal neurons with plasmids coding for m-htt exon 1 with different number of CAG repeats (18, 50 and 115) and demonstrated the influence of the length of polyQ sequence on neurite elongation. We found that exogenously applied FGF2 significantly rescued the m-htt-induced loss of neurite outgrowth. Moreover, the Enreptin peptide, an FGFR1 and NCAM dual agonist, had a similar neuritogenic effect to FGF2 in clinically relevant m-htt 50Q-expressing neurons. This study has developed an in vitro model of primary hippocampal neurons transfected with m-htt-coding vectors that is a powerful tool to study m-htt–related effects on neuronal placticity.

Original languageEnglish
JournalJournal of Neural Transmission
Volume126
Issue number11
Pages (from-to)1493-1500
ISSN0300-9564
DOIs
Publication statusPublished - Nov 2019

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Keywords

  • Enreptin
  • FGF2
  • Hippocampal neurons
  • Huntington disease
  • Mutant huntingtin
  • Neurite outgrowth

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