A Novel Microfluidic Device-Based Neurite Outgrowth Inhibition Assay Reveals the Neurite Outgrowth-Promoting Activity of Tropomyosin Tpm3.1 in Hippocampal Neurons

Stefen, H; Hassanzadeh-Barforoushi, A; Brettle, M; Fok, S; Suchowerska, AK; Tedla, N; Barber, T; Warkiani, ME; Fath, T

A Novel Microfluidic Device-Based Neurite Outgrowth Inhibition Assay Reveals the Neurite Outgrowth-Promoting Activity of Tropomyosin Tpm3.1 in Hippocampal Neurons

Stefen, H Hassanzadeh-Barforoushi, A Brettle, M Fok, S Suchowerska, AK Tedla, N Barber, T Warkiani, ME

Fath, T

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Publication Type:: Journal Article
Citation:: Cellular and Molecular Neurobiology, 2018, 38 (8), pp. 1557 - 1563
Issue Date:: 2018-11-01

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Field	Value	Language
dc.contributor.author	Stefen, H	en_US
dc.contributor.author	Hassanzadeh-Barforoushi, A	en_US
dc.contributor.author	Brettle, M	en_US
dc.contributor.author	Fok, S	en_US
dc.contributor.author	Suchowerska, AK	en_US
dc.contributor.author	Tedla, N	en_US
dc.contributor.author	Barber, T	en_US
dc.contributor.author	Warkiani, ME https://orcid.org/0000-0002-4184-1944	en_US
dc.contributor.author	Fath, T	en_US
dc.date.available	2018-09-06	en_US
dc.date.issued	2018-11-01	en_US
dc.identifier.citation	Cellular and Molecular Neurobiology, 2018, 38 (8), pp. 1557 - 1563	en_US
dc.identifier.issn	0272-4340	en_US
dc.identifier.uri	http://hdl.handle.net/10453/129081
dc.description.abstract	© 2018, Springer Science+Business Media, LLC, part of Springer Nature. Overcoming neurite inhibition is integral for restoring neuronal connectivity after CNS injury. Actin dynamics are critical for neurite growth cone formation and extension. The tropomyosin family of proteins is a regarded as master regulator of actin dynamics. This study investigates tropomyosin isoform 3.1 (Tpm3.1) as a potential candidate for overcoming an inhibitory substrate, as it is known to influence neurite branching and outgrowth. We designed a microfluidic device that enables neurons to be grown adjacent to an inhibitory substrate, Nogo-66. Results show that neurons, overexpressing hTpm3.1, have an increased propensity to overcome Nogo-66 inhibition. We propose Tpm3.1 as a potential target for promoting neurite growth in an inhibitory environment in the central nervous system.	en_US
dc.relation	http://purl.org/au-research/grants/arc/DP170103704
dc.relation	http://purl.org/au-research/grants/arc/DP180103003
dc.relation	http://purl.org/au-research/grants/nhmrc/GNT1143377
dc.relation.ispartof	Cellular and Molecular Neurobiology	en_US
dc.relation.isbasedon	10.1007/s10571-018-0620-7	en_US
dc.rights	info:eu-repo/semantics/closedAccess
dc.subject.classification	Neurology & Neurosurgery	en_US
dc.subject.mesh	Hippocampus	en_US
dc.subject.mesh	Neurons	en_US
dc.subject.mesh	Animals	en_US
dc.subject.mesh	Humans	en_US
dc.subject.mesh	Tropomyosin	en_US
dc.subject.mesh	Reproducibility of Results	en_US
dc.subject.mesh	Lab-On-A-Chip Devices	en_US
dc.subject.mesh	Nogo Proteins	en_US
dc.subject.mesh	Neuronal Outgrowth	en_US
dc.title	A Novel Microfluidic Device-Based Neurite Outgrowth Inhibition Assay Reveals the Neurite Outgrowth-Promoting Activity of Tropomyosin Tpm3.1 in Hippocampal Neurons	en_US
dc.type	Journal Article
utslib.citation.volume	8	en_US
utslib.citation.volume	38	en_US
utslib.for	1109 Neurosciences	en_US
utslib.for	0601 Biochemistry and Cell Biology	en_US
utslib.for	1115 Pharmacology and Pharmaceutical Sciences	en_US
pubs.embargo.period	Not known	en_US
pubs.organisational-group	/University of Technology Sydney
pubs.organisational-group	/University of Technology Sydney/Faculty of Engineering and Information Technology
pubs.organisational-group	/University of Technology Sydney/Faculty of Engineering and Information Technology/School of Biomedical Engineering
pubs.organisational-group	/University of Technology Sydney/Strength - CHT - Health Technologies
pubs.organisational-group	/University of Technology Sydney/Strength - IBMD - Initiative for Biomedical Devices
utslib.copyright.status	closed_access	*
pubs.issue	8	en_US
pubs.publication-status	Published	en_US
pubs.volume	38	en_US

Abstract:

© 2018, Springer Science+Business Media, LLC, part of Springer Nature. Overcoming neurite inhibition is integral for restoring neuronal connectivity after CNS injury. Actin dynamics are critical for neurite growth cone formation and extension. The tropomyosin family of proteins is a regarded as master regulator of actin dynamics. This study investigates tropomyosin isoform 3.1 (Tpm3.1) as a potential candidate for overcoming an inhibitory substrate, as it is known to influence neurite branching and outgrowth. We designed a microfluidic device that enables neurons to be grown adjacent to an inhibitory substrate, Nogo-66. Results show that neurons, overexpressing hTpm3.1, have an increased propensity to overcome Nogo-66 inhibition. We propose Tpm3.1 as a potential target for promoting neurite growth in an inhibitory environment in the central nervous system.

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http://hdl.handle.net/10453/129081