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

doi:10.1007/s00702-019-02073-1

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

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.

Originalsprog	Engelsk
Tidsskrift	Journal of Neural Transmission
Vol/bind	126
Udgave nummer	11
Sider (fra-til)	1493-1500
Antal sider	8
ISSN	0300-9564
DOI	https://doi.org/10.1007/s00702-019-02073-1
Status	Udgivet - 1 nov. 2019

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10.1007/s00702-019-02073-1

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FGF2 and dual agonist of NCAM and FGF receptor 1, Enreptin, rescue neurite outgrowth loss in hippocampal neurons expressing mutated huntingtin proteins. / Ilieva, Mirolyuba; Nielsen, Troels T.; Michel, Tanja et al.

I: Journal of Neural Transmission, Bind 126, Nr. 11, 01.11.2019, s. 1493-1500.

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › peer review

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

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.",

keywords = "Huntington disease, Mutant huntingtin, FGF2, Enreptin, Neurite outgrowth, Hippocampal neurons",

author = "Mirolyuba Ilieva and Nielsen, {Troels T.} and Tanja Michel and Stanislava Pankratova",

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T1 - FGF2 and dual agonist of NCAM and FGF receptor 1, Enreptin, rescue neurite outgrowth loss in hippocampal neurons expressing mutated huntingtin proteins

AU - Ilieva, Mirolyuba

AU - Nielsen, Troels T.

AU - Michel, Tanja

AU - Pankratova, Stanislava

PY - 2019/11/1

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N2 - 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.

AB - 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.

KW - Huntington disease

KW - Mutant huntingtin

KW - FGF2

KW - Enreptin

KW - Neurite outgrowth

KW - Hippocampal neurons

U2 - 10.1007/s00702-019-02073-1

DO - 10.1007/s00702-019-02073-1

M3 - Journal article

C2 - 31501979

SN - 0375-9245

VL - 126

SP - 1493

EP - 1500

JO - Acta Neurovegetativa

JF - Acta Neurovegetativa

IS - 11

ER -

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

Abstract

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