Relevant bibliographies by topics / Neurite regeneration

Academic literature on the topic 'Neurite regeneration'

Author: Grafiati
Published: 10 December 2022
Last updated: 21 February 2023

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Journal articles on the topic "Neurite regeneration"

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Walker, Sarah, Gaynor Spencer, Aleksandar Necakov, and Robert Carlone. "Identification and Characterization of microRNAs during Retinoic Acid-Induced Regeneration of a Molluscan Central Nervous System." International Journal of Molecular Sciences 19, no. 9 (September 13, 2018): 2741. http://dx.doi.org/10.3390/ijms19092741.

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Retinoic acid (RA) is the biologically active metabolite of vitamin A and has become a well-established factor that induces neurite outgrowth and regeneration in both vertebrates and invertebrates. However, the underlying regulatory mechanisms that may mediate RA-induced neurite sprouting remain unclear. In the past decade, microRNAs have emerged as important regulators of nervous system development and regeneration, and have been shown to contribute to processes such as neurite sprouting. However, few studies have demonstrated the role of miRNAs in RA-induced neurite sprouting. By miRNA sequencing analysis, we identify 482 miRNAs in the regenerating central nervous system (CNS) of the mollusc Lymnaea stagnalis, 219 of which represent potentially novel miRNAs. Of the remaining conserved miRNAs, 38 show a statistically significant up- or downregulation in regenerating CNS as a result of RA treatment. We further characterized the expression of one neuronally-enriched miRNA upregulated by RA, miR-124. We demonstrate, for the first time, that miR-124 is expressed within the cell bodies and neurites of regenerating motorneurons. Moreover, we identify miR-124 expression within the growth cones of cultured ciliary motorneurons (pedal A), whereas expression in the growth cones of another class of respiratory motorneurons (right parietal A) was absent in vitro. These findings support our hypothesis that miRNAs are important regulators of retinoic acid-induced neuronal outgrowth and regeneration in regeneration-competent species.
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Alhajlah, Sharif, Adam M. Thompson, and Zubair Ahmed. "Overexpression of Reticulon 3 Enhances CNS Axon Regeneration and Functional Recovery after Traumatic Injury." Cells 10, no. 8 (August 6, 2021): 2015. http://dx.doi.org/10.3390/cells10082015.

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CNS neurons are generally incapable of regenerating their axons after injury due to several intrinsic and extrinsic factors, including the presence of axon growth inhibitory molecules. One such potent inhibitor of CNS axon regeneration is Reticulon (RTN) 4 or Nogo-A. Here, we focused on RTN3 as its contribution to CNS axon regeneration is currently unknown. We found that RTN3 expression correlated with an axon regenerative phenotype in dorsal root ganglion neurons (DRGN) after injury to the dorsal columns, a well-characterised model of spinal cord injury. Overexpression of RTN3 promoted disinhibited DRGN neurite outgrowth in vitro and dorsal column axon regeneration/sprouting and electrophysiological, sensory and locomotor functional recovery after injury in vivo. Knockdown of protrudin, however, ablated RTN3-enhanced neurite outgrowth/axon regeneration in vitro and in vivo. Moreover, overexpression of RTN3 in a second model of CNS injury, the optic nerve crush injury model, enhanced retinal ganglion cell (RGC) survival, disinhibited neurite outgrowth in vitro and survival and axon regeneration in vivo, an effect that was also dependent on protrudin. These results demonstrate that RTN3 enhances neurite outgrowth/axon regeneration in a protrudin-dependent manner after both spinal cord and optic nerve injury.
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Yilmaz-Bayraktar, Suheda, Jana Schwieger, Verena Scheper, Thomas Lenarz, Ulrike Böer, Michaela Kreienmeyer, Mariela Torrente, and Theodor Doll. "Decellularized equine carotid artery layers as matrix for regenerated neurites of spiral ganglion neurons." International Journal of Artificial Organs 43, no. 5 (August 22, 2019): 332–42. http://dx.doi.org/10.1177/0391398819868481.

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Today’s best solution in compensating for sensorineural hearing loss is the cochlear implant, which electrically stimulates the spiral ganglion neurons in the inner ear. An optimum hearing impression is not ensured due to, among other reasons, a remaining anatomical gap between the spiral ganglion neurons and the implant electrodes. The gap could be bridged via pharmacologically triggered neurite growth toward the electrodes if biomaterials for neurite guidance could be provided. For this, we investigated the suitability of decellularized tissue. We compared three different layers (tunica adventitia, tunica media, and tunica intima) of decellularized equine carotid arteries in a preliminary approach. Rat spiral ganglia explants were cultured on decellularized equine carotid artery layers and neurite sprouting was assessed quantitatively. Generally, neurite outgrowth was possible and it was most prominent on the intima (in average 83 neurites per spiral ganglia explants, followed by the adventitia (62 neurites) and the lowest growth on the media (20 neurites). Thus, decellularized equine carotid arteries showed promising effects on neurite regeneration and can be developed further as efficient biomaterials for neural implants in hearing research.
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Lu, Wen, Margot Lakonishok, and Vladimir I. Gelfand. "Kinesin-1–powered microtubule sliding initiates axonal regeneration in Drosophila cultured neurons." Molecular Biology of the Cell 26, no. 7 (April 2015): 1296–307. http://dx.doi.org/10.1091/mbc.e14-10-1423.

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Understanding the mechanism underlying axon regeneration is of great practical importance for developing therapeutic treatment for traumatic brain and spinal cord injuries. Dramatic cytoskeleton reorganization occurs at the injury site, and microtubules have been implicated in the regeneration process. Previously we demonstrated that microtubule sliding by conventional kinesin (kinesin-1) is required for initiation of neurite outgrowth in Drosophila embryonic neurons and that sliding is developmentally down-regulated when neurite outgrowth is completed. Here we report that mechanical axotomy of Drosophila neurons in culture triggers axonal regeneration and regrowth. Regenerating neurons contain actively sliding microtubules; this sliding, like sliding during initial neurite outgrowth, is driven by kinesin-1 and is required for axonal regeneration. The injury induces a fast spike of calcium, depolymerization of microtubules near the injury site, and subsequent formation of local new microtubule arrays with mixed polarity. These events are required for reactivation of microtubule sliding at the initial stages of regeneration. Furthermore, the c-Jun N-terminal kinase pathway promotes regeneration by enhancing microtubule sliding in injured mature neurons.
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Ahmed, Morgan-Warren, Berry, Scott, and Logan. "Effects of siRNA-Mediated Knockdown of GSK3β on Retinal Ganglion Cell Survival and Neurite/Axon Growth." Cells 8, no. 9 (August 22, 2019): 956. http://dx.doi.org/10.3390/cells8090956.

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There are contradictory reports on the role of the serine/threonine kinase isoform glycogen synthase kinase-3β (GSK3β) after injury to the central nervous system (CNS). Some report that GSK3 activity promotes axonal growth or myelin disinhibition, whilst others report that GSK3 activity prevents axon regeneration. In this study, we sought to clarify if suppression of GSK3β alone and in combination with the cellular-stress-induced factor RTP801 (also known as REDD1: regulated in development and DNA damage response protein), using translationally relevant siRNAs, promotes retinal ganglion cell (RGC) survival and neurite outgrowth/axon regeneration. Adult mixed retinal cell cultures, prepared from rats at five days after optic nerve crush (ONC) to activate retinal glia, were treated with siRNA to GSK3β (siGSK3β) alone or in combination with siRTP801 and RGC survival and neurite outgrowth were quantified in the presence and absence of Rapamycin or inhibitory Nogo-A peptides. In in vivo experiments, either siGSK3β alone or in combination with siRTP801 were intravitreally injected every eight days after ONC and RGC survival and axon regeneration was assessed at 24 days. Optimal doses of siGSK3β alone promoted significant RGC survival, increasing the number of RGC with neurites without affecting neurite length, an effect that was sensitive to Rapamycin. In addition, knockdown of GSK3β overcame Nogo-A-mediated neurite growth inhibition. Knockdown of GSK3β after ONC in vivo enhanced RGC survival but not axon number or length, without potentiating glial activation. Knockdown of RTP801 increased both RGC survival and axon regeneration, whilst the combined knockdown of GSK3β and RTP801 significantly increased RGC survival, neurite outgrowth, and axon regeneration over and above that observed for siGSK3β or siRTP801 alone. These results suggest that GSK3β suppression promotes RGC survival and axon initiation whilst, when in combination with RTP801, it also enhanced disinhibited axon elongation.
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Sakane, Ayuko, Kazufumi Honda, and Takuya Sasaki. "Rab13 Regulates Neurite Outgrowth in PC12 Cells through Its Effector Protein, JRAB/MICAL-L2." Molecular and Cellular Biology 30, no. 4 (December 14, 2009): 1077–87. http://dx.doi.org/10.1128/mcb.01067-09.

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ABSTRACT Neurite outgrowth is the first step in the processes of neuronal differentiation and regeneration and leads to synaptic polarization and plasticity. Rab13 small G protein shows an increased mRNA expression level during neuronal regeneration; it is therefore thought to be involved in this process. We previously identified JRAB (junctional Rab13-binding protein)/MICAL-L2 (molecules interacting with CasL-like 2) as a novel Rab13 effector protein. Here, we show that Rab13 regulates neurite outgrowth in the rat pheochromocytoma cell line PC12 through an interaction with JRAB/MICAL-L2. The expression of JRAB/MICAL-L2 alone inhibits neurite outgrowth, whereas coexpression of the dominant active form of Rab13 rescues this effect. We also demonstrate an intramolecular interaction between the N-terminal calponin-homology (CH) and LIM domains of JRAB/MICAL-L2 and the C-terminal coiled-coil domain. Finally, we show that the binding of Rab13 to JRAB/MICAL-L2 stimulates the interaction of JRAB/MICAL-L2 with actinin-4, an actin-binding protein, which localizes to the cell body and the tips of the neurites in PC12 cells. These results suggest that Rab13 and JRAB/MICAL-L2 may act to transfer actinin-4 from the cell body to the tips of neurites, where actinin-4 is involved in the reorganization of the actin cytoskeleton which results in neurite outgrowth.
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Santos, Daniel, Francisco Gonzalez-Perez, Xavier Navarro, and Jaume del Valle. "Dose-Dependent Differential Effect of Neurotrophic Factors on In Vitro and In Vivo Regeneration of Motor and Sensory Neurons." Neural Plasticity 2016 (2016): 1–13. http://dx.doi.org/10.1155/2016/4969523.

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Although peripheral axons can regenerate after nerve transection and repair, functional recovery is usually poor due to inaccurate reinnervation. Neurotrophic factors promote directional guidance to regenerating axons and their selective application may help to improve functional recovery. Hence, we have characterized in organotypic cultures of spinal cord and dorsal root ganglia the effect of GDNF, FGF-2, NGF, NT-3, and BDNF at different concentrations on motor and sensory neurite outgrowth. In vitro results show that GDNF and FGF-2 enhanced both motor and sensory neurite outgrowth, NGF and NT-3 were the most selective to enhance sensory neurite outgrowth, and high doses of BDNF selectively enhanced motor neurite outgrowth. Then, NGF, NT-3, and BDNF (as the most selective factors) were delivered in a collagen matrix within a silicone tube to repair the severed sciatic nerve of rats. Quantification of Fluorogold retrolabeled neurons showed that NGF and NT-3 did not show preferential effect on sensory regeneration whereas BDNF preferentially promoted motor axons regeneration. Therefore, the selective effects of NGF and NT-3 shown in vitro are lost when they are applied in vivo, but a high dose of BDNF is able to selectively enhance motor neuron regeneration both in vitro and in vivo.
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Burstein, D. E., P. J. Seeley, and L. A. Greene. "Lithium ion inhibits nerve growth factor-induced neurite outgrowth and phosphorylation of nerve growth factor-modulated microtubule-associated proteins." Journal of Cell Biology 101, no. 3 (September 1, 1985): 862–70. http://dx.doi.org/10.1083/jcb.101.3.862.

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LiCl (2.5-20 mM) reversibly suppressed nerve growth factor (NGF)-induced neurite outgrowth by cultured rat PC 12 pheochromocytoma cells. Similar concentrations of LiCl also reversibly blocked NGF-dependent regeneration of neurites by PC12 cells that had been primed by long-term pre-exposure to NGF and by cultured newborn mouse sympathetic neurons. In contrast, transcription-dependent responses of PC12 cells to NGF such as priming and induction of the NGF-inducible large external glycoprotein, occurred despite the presence of Li+. SDS PAGE analysis of total cellular phosphoproteins (labeled by 2-h exposure to 32P-orthophosphate) from neurite-bearing primed PC12 cells revealed that Li+ reversibly inhibited the phosphorylation of a band of Mr 64,000 that was barely detectable in NGF-untreated PC12 cells. However, Li+ did not appear to affect the labeling of other phosphoproteins in either NGF-primed or untreated PC12 cultures, nor did it affect the rapid increase in phosphorylation of several proteins that occurs when NGF is first added to unprimed cultures. Several criteria indicated that the NGF-inducible phosphoprotein of Mr 64,000 is a microtubule-associated protein (MAP). Of the NGF-inducible phosphorylated MAPs that have been detected in PC12 cells (Mr 64,000, 72,000, 80,000, and 320,000), several (Mr 64,000, 72,000, and 80,000) were found to be substantially less phosphorylated in the presence of Li+. Neither a phorbol ester tumor promotor nor permeant cAMP analogs reversed the inhibitory effects of Li+ on neurite outgrowth or on phosphorylation of the component of Mr 64,000. Microtubules are a major and required constituent of neurites, and MAPs may regulate the assembly and stability of neuritic microtubules. The observation that Li+ selectively inhibits NGF-induced neurite outgrowth and MAP phosphorylation suggests a possible causal relationship between these two events.
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Nishiyama, N., K. Abe, H. Katsuki, and H. Saito. "Pharmacological analysis of neurite regeneration." Pathophysiology 1 (November 1994): 77. http://dx.doi.org/10.1016/0928-4680(94)90178-3.

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Gey, Manuel, Renate Wanner, Corinna Schilling, Maria T. Pedro, Daniela Sinske, and Bernd Knöll. "Atf3 mutant mice show reduced axon regeneration and impaired regeneration-associated gene induction after peripheral nerve injury." Open Biology 6, no. 8 (August 2016): 160091. http://dx.doi.org/10.1098/rsob.160091.

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Axon injury in the peripheral nervous system (PNS) induces a regeneration-associated gene (RAG) response. Atf3 (activating transcription factor 3) is such a RAG and ATF3's transcriptional activity might induce ‘effector’ RAGs (e.g. small proline rich protein 1a ( Sprr1a ) , Galanin ( Gal ) , growth-associated protein 43 ( Gap43 )) facilitating peripheral axon regeneration. We provide a first analysis of Atf3 mouse mutants in peripheral nerve regeneration. In Atf3 mutant mice, facial nerve regeneration and neurite outgrowth of adult ATF3-deficient primary dorsal root ganglia neurons was decreased. Using genome-wide transcriptomics, we identified a neuropeptide-encoding RAG cluster (vasoactive intestinal peptide ( Vip ) , Ngf, Grp, Gal, Pacap ) regulated by ATF3. Exogenous administration of neuropeptides enhanced neurite growth of Atf3 mutant mice suggesting that these molecules might be effector RAGs of ATF3's pro-regenerative function. In addition to the induction of growth-promoting molecules, we present data that ATF3 suppresses growth-inhibiting molecules such as chemokine (C-C motif) ligand 2. In summary, we show a pro-regenerative ATF3 function during PNS nerve regeneration involving transcriptional activation of a neuropeptide-encoding RAG cluster. ATF3 is a general injury-inducible factor, therefore ATF3-mediated mechanisms identified herein might apply to other cell and injury types.
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Dissertations / Theses on the topic "Neurite regeneration"

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Tan, Hiang Khoon. "Investigating the effects of TIMPs on excitotoxicity and neurite regeneration." Thesis, University of Bristol, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.247230.

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Witheford, Richter Miranda. "Olfactory ensheathing cell mediated mechanisms of neurite outgrowth and axon regeneration." Thesis, University of British Columbia, 2008. http://hdl.handle.net/2429/963.

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The capacity of the olfactory neuraxis to undergo neuronal replacement and axon targeting following injury, has led to scrutiny concerning the molecular and physical determinants of this growth capacity. This is because injury to the central nervous system, in contrast, leads to permanent disconnection of neurons with targets. Olfactory ensheathing cells (OECs), a specialized glial cell, may contribute to olfactory repair, and have been used to promote recovery from spinal cord injury. However, there mechanisms underlying OEC-induced regeneration are poorly appreciated. To understand these mechanisms, OECs from the lamina propria (LP OECs) or olfactory bulb (OB OECs) were transplanted into a lesion of the dorsolateral funiculus. While both cells demonstrated reparative capacities, LP and OB OECs differentially promoted spinal fibre growth; large-diameter neurofilament-positive, CGRP-positive, and serotonergic fibres sprouted in response to both LP and OB OEC transplantation, whereas substance-P and tyrosine hydroxylase-positive neurons grew more extensively following OB or LP OEC transplantation, respectively. To further understand the growth of spinal cord neurons in response to OECs, a proteomic analysis of OEC secreted factors was performed, identifying secreted protein acidic and rich in cysteines (SPARC) as a mediator of OEC-induced outgrowth in vitro. To test the contributions of SPARC to spinal cord repair after OEC transplantation, cultures of LP OECs from SPARC null and wildtype (WT) mice were transplanted into a crush of the dorsolateral funiculus. Substance P and tyrosine hydroxylase positive axon sprouting was significantly reduced in SPARC null OEC-treated animals, suggesting that individual factors may contribute to OEC-promoted regeneration. To investigate the effect of OECs on corticospinal (CST) neurons, an in vitro assay was developed using postnatal day 8 CST neurons. Coculture of CST neurons with OB OECs produced extensive axon elongation. Application of OB OEC secreted factors increased CST neurite branching, but did not increase axon elongation. In contrast, plating of CST neurons on OB OEC plasma membrane resulted in extensive axon elongation. Furthermore, the OB OEC plasma membrane could overcome CST neurite outgrowth inhibition induced by an outgrowth inhibitor. Together these findings provide insight into OEC mechanisms of neurite outgrowth and axon regeneration.
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Tam, Kin-wai, and 譚健偉. "Study of chondroitin sulphate abc lyases and their use in combination for promotion of neurite growth." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2010. http://hub.hku.hk/bib/B43571955.

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Chu, Gordon Kwok Tung. "The role of calcium in neuronal death and regeneration after neurite transection in a cell culture model." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape7/PQDD_0001/MQ46107.pdf.

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Wernicke, Catrin V. [Verfasser]. "Degeneration, Protektion und Regeneration dopaminerger Neurone / Catrin V. Wernicke." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2011. http://d-nb.info/1025239318/34.

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Ghaffari, Mithra. ""Glial Islands" promote survival and regeneration of neurites from chick embryo retinal neurons." CSUSB ScholarWorks, 1997. https://scholarworks.lib.csusb.edu/etd-project/1458.

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Fayaz, Imran. "Modeling axonal injury in vitro, injury, regeneration, and calcium dynamics following acute neuritic trauma." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp04/mq29281.pdf.

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Dinis, Tony Mickael. "Prothèse nerveuse artificielle à partir de fibroïne de soie pour la réparation et la régénération de nerfs périphériques." Thesis, Compiègne, 2014. http://www.theses.fr/2014COMP2152/document.

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La lésion de nerfs périphériques peut engendrer des déficits moteurs et/ou sensoriels permanents. En dépit des progrès techniques réalisés au cours de ces 25 dernières années, une récupération complète suite à ces lésions n’est pas encore possible aujourd'hui. L’autogreffe nerveuse, toujours considérée comme le standard clinique, est la seule technique capable d’offrir les meilleurs résultats en termes de récupération fonctionnelle. Cependant, la survenue de complications post-opératoires lors d’autogreffes d’un nerf et la quantité limitée de nerfs disponibles conduisent à mettre au point d’autres stratégies alternatives. Dans ce contexte, la mise au point de biomatériaux pour substituts nerveux devient une nécessité clinique. Malgré les efforts de la recherche, ces prothèses ne permettent toujours pas une régénération du nerf à la hauteur de l’autogreffe. Le biomatériau utilisé doit notamment présenter des propriétés physiques et chimiques proches de celui du nerf natif. La soie, aux propriétés mécaniques uniques, représente une bonne alternative pour mettre au point ce type de prothèses. En effet, la protéine de soie déjà utilisée dans le domaine biomédical est biocompatible. Les modifications chimiques de cette protéine améliore et favorise l’adhérence et la croissance cellulaires par l’incorporation de facteurs de croissance ou d’autres molécules d'intérêt. Ce travail de thèse propose de développer un nouveau type de biomatériau à base de soie fonctionnalisée par deux facteurs de croissance : le Nerve Growth Factor (NGF) et le Ciliary NeuroTrophic Factor (CNTF). Étant donné l’architecture complexe qui compose la structure nerveuse, une matrice supportant la repousse des tissus de façon orientée semble primordiale. Nous démontrons, dans un premier temps, le pouvoir de ces nanofibres alignées (produites par electrospinning) à orienter la régénération tissulaire de différents organes par culture d’explants. Les nanofibres de soie alignées, biocompatibles sont bio-activées par ajout de NGF spécifique de la régénération nerveuse. Cette matrice créée présente un gradient de concentration en NGF qui permet d’orienter la repousse axonale en stimulant la croissance axonale dans une seule direction. Afin d’optimiser la croissance de deux populations cellulaires, nous avons incorporé du CNTF pour produire des nanofibres bifonctionnalisées. Ces nanofibres bifonctionnalisées ont conduit à une longueur des neurites 3 fois plus grande à leurs contacts, stimulant la croissance des cellules gliales. Ainsi, nous avons produit des conduits nerveux à base de soie biofonctionnalisée pour implantation chez le rat. Les analyses physico-chimiques et les propriétés mécaniques démontrent le caractère biomimétique de nos tubes de guidage. Les premières études de la locomotion et l’observation de coupes du nerf sciatique de rat, suite à l’implantation de nos conduits donnent des résultats très prometteurs. L’ensemble de ces travaux démontre l’efficacité de nos guides nerveux à base de soie et les présente comme une alternative prometteuse à l’autogreffe nerveuse pratiquée en clinique
Peripheral nerve injury causes sensory and/or motor functions deficits. Despite technological advances over the past 25 years, a complete recovery from these injuries remains unsatisfactory today. The autograft still considered the "gold standard" in clinical practice. This is the only technique able to offer complete functional recovery. However, the occurrence of postoperative complications in autologous nerve and the limited amount of available nerves lead to develop alternatives strategy.In this context, development of nerve graft substitutes becomes by far a clinical necessity. Despite research efforts, these artificial prostheses design based on biomaterial doesn’t allow nerve regeneration as found in autograft nerve procedures. The biomaterial used must have the physical and chemical properties similar to that of the native nerve. Silk, well known for its unique mechanical properties, proposes a good alternative to develop these prostheses. Indeed, the silk protein is commonly used in the biomedical field and regenerative medicine. This protein biocompatibility may be improved through chemical modifications to promote adhesion and cell growth by the incorporation of growth factors or other molecules of interest. Therefore, this thesis proposes to develop a new type of functionalized silk biomaterial based on two growth factors : Nerve Growth Factor (NGF) and Ciliary NeuroTrophic Factor (CNTF). Given the complex architecture that consists of nerve structure, a matrix which is able to support and manage the outgrowth of tissue becomes essential. We demonstrate the power of these aligned nanofibers (produced by electrospinning) to guide and manage tissue regeneration from different organ explants culture. Aligned silk nanofibers, were biocompatible and bio-activated by adding NGF involved for nerve regeneration. This matrix has been created with a concentration gradient of NGF to guide neuritis outgrowth in only one direction. The presence of this gradient demonstrated a better axonal growth in one direction versus the uniform concentration conditions. Nerve cells consist essentially of two cell populations which are neurons and Schwann cells. To optimize the culture and growth of these two populations, in addition to NGF, we incorporated CNTF to produce bifunctionalized nanofibers. These biofunctionalised nanofibers led to a length 3 times larger on contact with neurites. The glial cells growth, alignment and migration were stimulated by CNTF. Thus, we produced bi-functionalized nerve guidance conduits for rat implantation. The physico-chemical analyzes demonstrate the biomimetic of our guide tubes. Early studies of locomotion and observing histological sections of rat sciatic nerve, following the implementation of our conduits gave very promising results.These studies demonstrate the relevance of our nervous guides’ silk-based developed as an effective alternative to nerve autograft performed in the clinic
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Jerregård, Helena. "Factors influencing nerve growth in situ and in vitro /." Linköping : Univ, 2001. http://www.bibl.liu.se/liupubl/disp/disp2001/med693s.pdf.

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Mille-Hamard, Laurence. "Transplantation de ganglions rachidiens fœtaux et adultes dans la moelle épinière et dans le nerf péronier du rat adulte : survie, expression phénotypique et capacité de repousse axonale des neurones sensoriels primaires qui y sont contenus." Paris 5, 1997. http://www.theses.fr/1997PA05S031.

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Apres lésion traumatique de la moelle épinière, une restructuration médullaire complète nécessite non seulement le rétablissement du versant efférent, moteur, mais aussi de celui du versant affèrent, sensitif. Dans une approche de recherche fondamentale susceptible de s'ouvrir sur des perspectives cliniques, nous avons transplante, chez le rat adulte, des ganglions rachidiens cervicaux fœtaux et adultes : 1) dans le nerf péronier ; 2) dans la moelle épinière cervicale. Dans le cas des seules transplantations intramédullaires de ganglions adultes, nous avons réalisé trois variantes : a) ganglion(s) seul(s) ; b) ganglion connectée à un autogreffon de nerf périphérique (gnp) ; c) ganglion relie, au moyen d'un gnp, a un muscle squelettique préalablement dénervé. Chez le rat adulte, nous avons estimé à 7000 le nombre de neurones sensoriels primaires dans les ganglions rachidiens cervicaux 4, 5 et 6. Transplantes dans le système nerveux périphérique, 20% de ces neurones survivent. Dans la moelle épinière, les ganglions sont biens tolérés, mais seuls 5% des neurones sensoriels primaires survivent à la transplantation, leurs caractéristiques phénotypiques sont modifiées. La présence d'éléments nerveux périphériques permet la survie d'un plus grand nombre de neurones, en particulier ceux de plus grand diamètre. De façon surprenante, la survie des neurones sensoriels primaires fœtaux est inférieure à celle des neurones adultes. Les neurones sensoriels primaires fœtaux et adultes transplantes sont capables de régénérer, et certains de façon bidirectionnelle, dans le système nerveux périphérique. On en conclut que les neurones sensoriels primaires des ganglions rachidiens, tant adultes que fœtaux, peuvent être transplantes dans le système nerveux central et dans le système nerveux périphérique du rat adulte. Dans une perspective thérapeutique de réparation médullaire post-traumatique, il conviendrait de préciser le degré d'intégration anatomique et fonctionnelle des transplants et de rechercher de nouvelles stratégies (facteurs neurotrophiques, thérapie génique, etc. ) permettant d'augmenter le taux de survie des neurones sensoriels transplantes.
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Books on the topic "Neurite regeneration"

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Chu, Gordon Kwok Tung. The role of calcium in neuronal death and regeneration after neurite transection in a cell culture model. Ottawa: National Library of Canada, 1999.

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Takao, Kumazawa, Kruger Lawrence, and Mizumura Kazue, eds. The polymodal receptor: A gateway to pathological pain. Amsterdam: Elsevier, 1996.

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Motor Neurone Disease. Taylor & Francis Group, 2017.

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Hunter, Margaret, and Ian Robinson. Motor Neurone Disease. Taylor & Francis Group, 2005.

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Hunter, Margaret, and Ian Robinson. Motor Neurone Disease. Taylor & Francis Group, 2005.

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Hunter, Margaret, and Ian Robinson. Motor Neurone Disease. Taylor & Francis Group, 2005.

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Hunter, Margaret, and Ian Robinson. Motor Neurone Disease. Taylor & Francis Group, 2005.

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Modeling axonal injury in vitro: Injury, regeneration, and calcium dynamics following acute neuritic trauma. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1999.

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(Editor), T. Kumazawa, L. Kruger (Editor), and K. Mizumura (Editor), eds. The Polymodal Receptor - A Gateway to Pathological Pain (Progress in Brain Research). Elsevier Science, 1996.

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Book chapters on the topic "Neurite regeneration"

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Monard, D. "Rate Limiting Events in Neurite Outgrowth." In Neural Development and Regeneration, 115–24. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-73148-8_11.

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Rauvala, Heikki, Yrjö Mähönen, Jukkapekka Jousimaa, Jussi Merenmies, Dan Lindholm, and Matti Vuento. "Neurite Outgrowth Induced by Adhesive Proteins." In Glial-Neuronal Communication in Development and Regeneration, 159–81. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-71381-1_12.

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Henderson, Christopher E. "Neurite-Promoting Factors for Spinal Neurons." In Glial-Neuronal Communication in Development and Regeneration, 407–17. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-71381-1_25.

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Michler, A., and J. R. Wolff. "Modulation of Neurite Growth by Gaba in Cell Culture." In Neural Development and Regeneration, 665–66. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-73148-8_67.

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Beckh, Synnöve, Hans Werner Müller, and Wilfried Seifert. "Neurotrophic and Neurite Promoting Activities in Astroglial Conditioned Medium." In Glial-Neuronal Communication in Development and Regeneration, 385–406. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-71381-1_24.

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Yavin, E., S. Gil, G. Guroff, T. Hama, and C. Richter-Landsberg. "Glycoconjugate Metabolism, Accretion and Release During Neurite Outgrowth in Normal and Transformed Cells of Neuronal Origin." In Glial-Neuronal Communication in Development and Regeneration, 303–21. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-71381-1_19.

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Unsicker, Klaus, and Rolf Lietzke. "Chromaffin Cells: Modified Neurons that are Both Targets and Storage Sites of Neuronotrophic and Neurite Promoting Factors." In Glial-Neuronal Communication in Development and Regeneration, 365–84. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-71381-1_23.

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Doherty, Patrick, John G. Dickson, Thomas P. Flanigan, and Frank S. Walsh. "Molecular Specificity of Ganglioside Action on Neurite Regeneration in Cell Cultures of Sensory Neurons." In Gangliosides and Neuronal Plasticity, 335–46. New York, NY: Springer New York, 1986. http://dx.doi.org/10.1007/978-1-4757-5309-7_27.

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Tsang, Chi Kwan, and Yuto Kamei. "Long Term Neurite Outgrowth Enhancing Effect and Neurite Regeneration Effect of an Active Substance from a Brown Alga Sargassum Macrocarpum on Rat Pheochromocytoma PC12D Cells." In Animal Cell Technology: Basic & Applied Aspects, 407–13. Dordrecht: Springer Netherlands, 2002. http://dx.doi.org/10.1007/978-94-017-0728-2_71.

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Kosik, K. S. "The Neuritic Dystrophy of Alzheimer’s Disease: Degeneration or Regeneration?" In Growth Factors and Alzheimer’s Disease, 234–40. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-46722-6_20.

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Conference papers on the topic "Neurite regeneration"

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Sundararaghavan, Harini G., Gary A. Monteiro, and David I. Shreiber. "Microfluidic Generation of Adhesion Gradients Through 3D Collagen Gels: Implications for Neural Tissue Engineering." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192987.

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During development, neurites are directed by gradients of attractive and repulsive soluble (chemotactic) cues and substrate-bound adhesive (haptotactic) cues. Many of these cues have been extensively researched in vitro, and incorporated into strategies for nerve and spinal cord regeneration, primarily to improve the regenerative environment. To enhance and direct growth, we have developed a system to create 1D gradients of adhesion through a 3D collagen gel using microfluidics. We test our system using collagen grafted with bioactive peptide sequences, IKVAV and YIGSR, from laminin — an extra-cellular matrix (ECM) protein known to strongly influence neurite outgrowth [1, 2]. Gradients are established from 0.14 mg/ml–0, and 0.07 mg/ml–0 of each peptide and tested using chick dorsal root ganglia (DRG). Neurite growth is evaluated 5 days after gradient formation. Neurites show increased growth in the gradient system when compared to control and biased growth up the gradient of peptides. These results demonstrate that neurite growth can be enhanced and directed by controlled, immobilized, haptotactic gradients through 3D scaffolds, and suggest that including these gradients in regenerative therapies may accelerate nerve and spinal cord regeneration.
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Sundararaghavan, Harini G., Gary A. Monteiro, and David I. Shreiber. "Guided Axon Growth by Gradients of Adhesion in Collagen Gels." In ASME 2008 International Mechanical Engineering Congress and Exposition. ASMEDC, 2008. http://dx.doi.org/10.1115/imece2008-69124.

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During development, neurites are directed by gradients of attractive and repulsive soluble (chemotactic) cues and substrate-bound adhesive (haptotactic) cues. Many of these cues have been extensively researched in vitro, and incorporated into strategies for nerve and spinal cord regeneration, primarily to improve the regenerative environment. To enhance and direct growth, we have developed a system to create 1D gradients of adhesion through a 3D collagen gel using microfluidics. We test our system using collagen grafted with bioactive peptide sequences, IKVAV and YIGSR, from laminin — an extra-cellular matrix (ECM) protein known to strongly influence neurite outgrowth. Gradients are established from ∼0.37mg peptide/mg collagen – 0, and ∼0.18 mg peptide/mg collagen – 0 of each peptide and tested using chick dorsal root ganglia (DRG). Neurite growth is evaluated 5 days after gradient formation. Neurites show increased growth in the gradient system when compared to control and biased growth up the gradient of peptides. Growth in YIGSR-grafted collagen increased with steeper gradients, whereas growth in IKVAV-grafted collagen decreased with steeper gradients. These results demonstrate that neurite growth can be enhanced and directed by controlled, immobilized, haptotactic gradients through 3D scaffolds, and suggest that including these gradients in regenerative therapies may accelerate nerve and spinal cord regeneration.
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Sundararaghavan, Harini G., and David I. Shreiber. "Directing Neurite Growth in 3D Collagen Scaffolds With Gradients of Mechanical Properties." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176659.

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Biomaterial scaffolds for nerve and spinal cord regeneration must not only promote neurite re-growth but also direct it. Several cell types, including neurons, respond to the mechanical properties of the substrate on which they are grown. We believe that gradients of mechanical properties can be used to direct neurons. To spatially control the mechanical properties, gradients of genipin — a naturally occurring, cell-tolerated crosslinking agent — are created in 3D through a compliant collagen gel using microfluidics. Gradients of mechanical properties are evaluated by measuring genipin-induced fluorescence, which we have previously correlated to mechanical properties. Growth of neurites was evaluated in gels of uniform stiffness and a gradient generated by incubation in 0 to 1 mM genipin for 12hrs to produce approximately an order of magnitude change in the shear modulus. Neurite growth was evaluated 5 days after gradient formation. Neurites demonstrated a directional bias against the gradient of stiffness. These results demonstrate that neurites can respond to subtle gradients of mechanical properties within a 3D scaffold and point to opportunities to manipulate properties for directed nerve and spinal cord regeneration.
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Sundararaghavan, Harini G., and David I. Shreiber. "Gradients of Stiffness Guide Neurite Growth in 3D Collagen Gels." In ASME 2007 International Mechanical Engineering Congress and Exposition. ASMEDC, 2007. http://dx.doi.org/10.1115/imece2007-41873.

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One approach to enhance nerve and spinal cord regeneration following injury is to implant a biomaterial scaffold to ”bridge” the gap of the injury. Structural/mechanical anisotropy has been suggested as a means of orienting this growth axially. We have spatially varied the mechanical properties of a 3D collagen gel to direct growth axially and unidirectionally. Gradients of mechanical properties were generated in collagen gels by exposing the collagen to a 0–1mM gradient of genipin, a cell-tolerated crosslinking agent, for 12hrs via microfluidics. The gradient of stiffness was confirmed via a gradient of genipin-induced fluorescence intensity, which we have previously correlated to the storage modulus of collagen gels. The growth of neurites from isolated chick embryo dorsal root ganglia (DRG) in the presence of these gradients was evaluated after 5 days in culture. In control cases, neurites grew into the collagen gel and up either side of the cross-channel to approximately equal lengths. A 20% difference in differential growth was observed in control experiments. In contrast, when presented a gradient of shear modulus from ∼365Pa – 60Pa, neurites elected to grow down the gradient of stiffness to the compliant side, with an almost 300% difference. Interestingly, the length of neurites in gels with gradients was significantly greater than the length of those grown in gels with uniform, untreated gels with high compliance. Control of neurite growth, cell migration, and other aspects of cell behavior in 3D scaffolds via mechanical properties offers vast potential for tissue engineering and other regenerative therapies.
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Schwieger, J., N. Kakuan, A. Osorio-Madrazo, T. Lenarz, and V. Scheper. "Neurite regeneration of primary auditory neurons in hydrogels." In Abstract- und Posterband – 90. Jahresversammlung der Deutschen Gesellschaft für HNO-Heilkunde, Kopf- und Hals-Chirurgie e.V., Bonn – Digitalisierung in der HNO-Heilkunde. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1686893.

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Lee, Se-Jun, Wei Zhu, and Lijie Grace Zhang. "Development of Novel 3D Scaffolds With Embedded Core-Shell Nanoparticles for Nerve Regeneration." In ASME 2015 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2015. http://dx.doi.org/10.1115/imece2015-51595.

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Neural tissue engineering has emerged as a promising alternative to address various nerve injuries. Particularly, advancement in both 3D biomimetic scaffold fabrication strategies and nanotechnology has inspired this field into a new era. In this study, we fabricated a novel 3D biomimetic scaffold, which has tunable porous structure and embedded core-shell nanoparticles with neurogenic factor delivery system, using stereolithography (SL) based 3D printing and core-shell electrospraying techniques. Our results indicated that scaffolds with higher porosity significantly improve PC-12 neural cell adhesion compared to ones with smaller porosity. Furthermore, scaffolds embedded bovine serum albumin (BSA) containing nanoparticles showed an enhancement in cell proliferation relative to bared control scaffolds. In addition, confocal microscopy images illustrated that the scaffold with nerve growth factor (NGF) nanoparticles increased the length of neuritis and directed neurite extension of PC-12 cells along the fiber. The results in this study demonstrate the potential of this 3D scaffold in improving neural cell function and nerve growth.
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Arcaute, K., L. Ochoa, B. K. Mann, and R. B. Wicker. "Stereolithography of PEG Hydrogel Multi-Lumen Nerve Regeneration Conduits." In ASME 2005 International Mechanical Engineering Congress and Exposition. ASMEDC, 2005. http://dx.doi.org/10.1115/imece2005-81436.

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Peripheral nerve regeneration conduits available today are single lumen conduits. Multi-lumen conduits offer advantages over currently available conduits in that multiple lumen better mimic the natural structure of the nerve, provide a greater surface area for neurite extension, and allow for more precisely located growth factors or support cells within the scaffold. This work describes and demonstrates the use of the stereolithography (SL) rapid prototyping technique for fabricating multi-lumen nerve guidance conduits (NGCs) out of photopolymerizable poly(ethylene glycol) (PEG). NGCs were fabricated from PEG-dimethacrylate (PEG-dma) molecular weight 1000 with 30% (w/v) aqueous solution and 0.5% (w/v) of the photoinitiator Irgacure 2959. The selection of the PEG-dma and photoinitiator concentration was based on previous work [13]. A 3D Systems 250/50 SL machine with a 250 μm laser beam diameter was used for the experiments in a slightly modified process where the NGCs were fabricated on a glass slide within a small flat-bottom cylindrical container placed on top of the SL machine’s original build platform. SL successfully manufactured three-dimensional, multi-layered and multi-material NGCs with varying overall NGC lengths and lumen sizes. Minimum lumen size, spacing, and geometric accuracy were constrained by the laser beam diameter and path, curing characteristics of the polymer solution, and UV transmission properties of the polymer solution and cured PEG-dma. Overall lengths of the NGCs were constrained by the ability of the conduit to self-support its own construction. Multiple material conduits were demonstrated by varying the build solution during the layering process. In summary, SL shows promise for fabrication of bioactive NGCs using PEG hydrogels, and the use of SL in this application offers the additional advantage of easily scaling up for mass production.
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Masand, Shirley, Jian Chen, Melitta Schachner, and David I. Shreiber. "A Bioactive Peptide Grafted Scaffold for Peripheral Nerve Regeneration." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53627.

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Despite this innate regenerative potential of the peripheral nervous system, functional recovery often remains incomplete, especially as the severity of injury increases. This has been attributed to a number of sources including the ingrowth of fibrous scar tissue, lack of mechanical support for emerging neurites, and the malrouted reinnervation of neurites towards inappropriate targets. While research in the field is broad, it is generally accepted that an optimal nerve guidance conduit to encourage regeneration should include both biological and mechanical support for emerging neurites and glia.
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Masand, Shirley, Jian Chen, Melitta Schachner, and David I. Shreiber. "Functionalized Collagen Scaffolds for Peripheral Nerve Regeneration." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19680.

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Despite the robust regenerative potential of the peripheral nervous system, a permanent loss of function is often associated with injury. A multitude of causes have been implicated in this outcome, including the presence of a non-permissive microenvironment surrounding the injury and the regrowth of emerging neurites towards inappropriate targets. Preferential motor reinnervation is a naturally occurring phenomenon where motor axons have increased accuracy in reaching their appropriate end targets as the course of regeneration proceeds1. Several molecules have been implicated in encouraging this response, including two carbohydrates — Polysialic Acid (PSA) and Human Natural Killer Epitope-1 (HNK-1)2,3. Peptide mimics of these molecules have been identified4,5, which are more stable and economical than their glycan counterparts, and have independently been shown to enhance PMR in a soluble form, but only for transection distances substantially smaller than the 5-mm ‘critical gap’ size for mice6,7.
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Todorovic, Natasa, Gordana Stojadinovic, Kamal AlJamal, and Miroslav Zivic. "THE MORPHOMETRIC STUDY OF THE EFFECTS OF BISPEROXOVANADIUM (BPV(PHEN)) ON NEONATAL DRG NEURONS IN CULTURE." In 1st INTERNATIONAL Conference on Chemo and BioInformatics. Institute for Information Technologies, University of Kragujevac,, 2021. http://dx.doi.org/10.46793/iccbi21.214t.

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Unlike the neurons in the CNS, the peripheral neurons have certain intrinsic regenerative capacity. After injury, peripheral neurons can switch to a cellular “state for growth”, with the expression profiles similar to early developmental stages. We looked at the changes of morphometric parameters induced in young peripheral neurons with treatments that in adult neurons have growth-stimulatory effect. The experimental treatments compared to control were: BpV (phen), an inhibitor of PTEN; and bFGF, basic fibroblast growth factor. The neurite growth was measured on cultured dissociated dorsal root ganglia neonatal neurons fixed 24h after treatment and immunostained with anti-neurofilament H (NF-H) phosphorylated antibody. FIJI Simple Neurite Tracer was used for morphometry of individual neurons. 24h post treatment, compared to control, total neurite length, length of primary and length of terminal branches, were increased by bFGF but not by BpV treatment. In all measured parameters related to the degree of branching, BpV- treated neurons had small dispersion of values and small mean values, reminiscent of literature data stating that BpV treated neurons are elongated and less branched. However, the BpV did not have a positive influence on neurite elongation, as was reported on adult neurons. In contrast, bFGF stimulated elongation of young neurons in the manner similar to the effects described on the adult neurons.
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