| Literature DB >> 30218404 |
Holly Stefen1,2, Amin Hassanzadeh-Barforoushi3,4, Merryn Brettle1, Sandra Fok1, Alexandra K Suchowerska1, Nicodemus Tedla5, Tracie Barber3, Majid Ebrahimi Warkiani6,7, Thomas Fath8,9,10.
Abstract
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.Entities:
Keywords: Microfluidic systems; Neurite outgrowth inhibition; NogoA; Tropomyosins
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Year: 2018 PMID: 30218404 DOI: 10.1007/s10571-018-0620-7
Source DB: PubMed Journal: Cell Mol Neurobiol ISSN: 0272-4340 Impact factor: 5.046