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Search Results: 1 - 10 of 2165 matches for " Axon regeneration "
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Induced-pluripotent stem cells seeded acellular peripheral nerve graft as “autologous nerve graft”  [PDF]
Jiang Li, Guo-Dong Gao, Ti-Fei Yuan
Journal of Biomedical Science and Engineering (JBiSE) , 2010, DOI: 10.4236/jbise.2010.31012
Abstract: The hypothesis is that induced pluripotent stem cells (iPSC) derived Schwann cells and/or macrophages can be transplanted into acellular nerve graft in repairing injured nervous system. The efficiency of iPSC seeded acellular nerve graft may mimic the autologous peripheral nerve graft.
Immunohistochemical Distribution of PlexinA4 in the Adult Rat Central Nervous System
Claire-Anne Gutekunst,Eric N. Stewart,Robert E. Gross
Frontiers in Neuroanatomy , 2010, DOI: 10.3389/fnana.2010.00025
Abstract: PlexinA4 is the latest member to be identified of the PlexinA subfamily, critical transducers of class 3 semaphorin signaling as co-receptors to neuropilins 1 and 2. Despite functional information regarding the role of PlexinA4 in development and guidance of specific neuronal pathways, little is known about its distribution in the adult central nervous system (CNS). Here we report an in depth immunohistochemical analysis of PlexinA4 expression in the adult rat CNS. PlexinA4 staining was present in neurons and fibers throughout the brain and spinal cord, including neocortex, hippocampus, lateral hypothalamus, red nucleus, facial nucleus, and the mesencephalic trigeminal nucleus. PlexinA4 antibodies labeled fibers in the lateral septum, nucleus accumbens, several thalamic nuclei, substantia nigra pars reticulata, zona incerta, pontine reticular region, as well as in several cranial nerve nuclei. This constitutes the first detailed description of the topographic distribution of PlexinA4 in the adult CNS and will set the basis for future studies on the functional implications of PlexinA4 in adult brain physiology.
EphB2 signaling regulates lesion-induced axon sprouting but not critical period length in the postnatal auditory brainstem
Nakamura Paul A,Cramer Karina S
Neural Development , 2013, DOI: 10.1186/1749-8104-8-2
Abstract: Background Studies of developmental plasticity may provide insight into plasticity during adulthood, when neural circuitry is less responsive to losses or changes in input. In the mammalian auditory brainstem, globular bushy cell axons of the ventral cochlear nucleus (VCN) innervate the contralateral medial nucleus of the trapezoid body (MNTB) principal neurons. VCN axonal terminations in MNTB, known as calyces of Held, are very large and specialized for high-fidelity transmission of auditory information. Following unilateral deafferentation during postnatal development, VCN axons from the intact side form connections with novel targets, including the ipsilateral MNTB. EphB signaling has been shown to play a role in this process during the first postnatal week, but mechanisms involved in this reorganization during later developmental periods remain unknown. Results We found that EphB2 signaling reduces the number of induced ipsilateral projections to the MNTB after unilateral VCN removal at postnatal day seven (P7), but not after removal of the VCN on one side at P10, after the closure of the critical period for lesion-induced innervation of the ipsilateral MNTB. Conclusions Results from this study indicate that molecular mechanisms involved in the development of circuitry may also play a part in rewiring after deafferentation during development, but do not appear to regulate the length of critical periods for plasticity.
Rho-independent stimulation of axon outgrowth and activation of the ERK and Akt signaling pathways by C3 transferase in sensory neurons
Rüdiger Schweigreiter,Sitthisak Thongrong,Markus H?ltje,Lars Klimaschewski
Frontiers in Cellular Neuroscience , 2012, DOI: 10.3389/fncel.2012.00043
Abstract: Peripheral nerve injury triggers the activation of RhoA in spinal motor and peripheral sensory neurons. RhoA activates a number of effector proteins including the Rho-associated kinase, ROCK, which targets the cytoskeleton and leads to inhibition of neurite outgrowth. Blockade of the Rho/ROCK pathway by pharmacological means improves axon regeneration after experimental injury. C3bot transferase, an exoenzyme produced by Clostridium botulinum, inactivates RhoA by ADP-ribosylation. It has been successfully applied in experimental CNS lesions to facilitate axon regeneration. Up to now it was not investigated thoroughly whether C3bot exerts positive effects on peripheral axon regeneration as well. In the present study, recombinant membrane permeable C3bot produced a small, but significant, axon outgrowth effect on peripheral sensory neurons dissociated from adult dorsal root ganglia (DRG) of the rat. Neuronal overexpression of C3, however, did not enhance axonal growth. Moreover, transfection of plasmids encoding dominant negative RhoA or RhoA specific shRNAs failed to increase axonal growth. Furthermore, we show that the C3bot mutant, C3E174Q, which lacks RhoA inhibitory activity, still stimulates axonal growth. When analyzing possible signaling mechanisms we found that extracellular signal-regulated kinase (ERK) and Akt are activated by C3bot and ERK is induced by the C3E174Q mutant. Upregulation of kinase activities by C3bot occurs significantly faster than inactivation of RhoA indicating a RhoA-independent pathway of action by C3bot. The induction of ERK signaling by C3bot was detected in embryonic hippocampal neurons, too. Taken together, although RhoA plays a central role for inhibition of axon outgrowth by myelin-derived inhibitors, it does not interfere with axonal growth of sensory neurons on a permissive substrate in vitro. C3bot blocks neuronal RhoA activity, but its positive effects on axon elongation and branching appear to be mediated by Rho independent mechanisms involving activation of axon growth promoting ERK and Akt kinases.
The effect of glial fibrillary acidic protein expression on neurite outgrowth from retinal explants in a permissive environment
Kimberly A Toops, Tracy L Hagemann, Albee Messing, Robert W Nickells
BMC Research Notes , 2012, DOI: 10.1186/1756-0500-5-693
Abstract: Explants from Gfap-/- and Gfap+/- mice did not have increased neurite outgrowth compared with Gfap+/+ or Gfap over-expressing mice as would be expected if GFAP was detrimental to axon regeneration. In fact, Gfap over-expressing explants had the most neurite outgrowth when treated with a neurite stimulatory media. Transmission electron microscopy revealed that neurites formed bundles, which were surrounded by larger cellular processes that were GFAP positive indicating a close association between growing axons and glial cells in this regeneration paradigm.We postulate that glial cells with increased Gfap expression support the elongation of new neurites from retinal ganglion cells possibly by providing a scaffold for outgrowth.Within the central nervous system, glial cells provide critical support for neurons. Due to the intertwined nature of glial and neuronal interactions and functions, when neurons are injured, as the retina ganglion cells (RGCs) are in glaucoma, glial cells also react and undergo morphological changes and alterations in gene expression [1-5].After optic nerve injury astrocytes surrounding the optic nerve head become reactive and are intimately involved with formation of glial scar tissue in the optic nerve. The glial scar strongly inhibits axon regeneration from the RGCs and may contribute to further axon damage leading to RGC death and irreversible blindness [6-8]. Müller cells respond to optic nerve injury by increasing their expression of glutamine synthetase [9] and the growth factor ciliary neurotrophic factor [10]. One common feature of both astrocyte and Müller cell reactivity (and glial cell reactivity in general) is the increased expression of glial fibrillary acidic protein (GFAP) [9,11-17]. GFAP is a type III intermediate filament protein component of the cytoskeleton. Astrocytes constitutively express GFAP, while mature Müller cells normally do not express GFAP [1,3].Beyond GFAP’s function as a cytoskeleton component, its role within
Serum response factor modulates neuron survival during peripheral axon injury
Sina Stern, Daniela Sinske, Bernd Knoll
Journal of Neuroinflammation , 2012, DOI: 10.1186/1742-2094-9-78
Abstract: Here, we demonstrate that upon neuronal injury, that is facial nerve transection, constitutively-active SRF-VP16 enhances motorneuron survival. SRF-VP16 suppressed active caspase 3 abundance in vitro and enhanced neuron survival upon camptothecin induced apoptosis. Following nerve fiber injury in vitro, SRF-VP16 improved survival of neurons and re-growth of severed neurites. Further, SRF-VP16 enhanced immune responses (that is microglia and T cell activation) associated with neuronal injury in vivo. Genome-wide transcriptomics identified target genes associated with axonal injury and modulated by SRF-VP16.In sum, this is a first report describing a neuronal injury-related survival function for SRF.
Local regulation of the axonal phenotype, a case of merotrophism
Biological Research , 2005, DOI: 10.4067/S0716-97602005000400009
Abstract: in this essay, we show that several anatomical features of the axon, namely, microtubular content, caliber and extension of sprouts, correlate on a local basis with the particular condition of the glial cell, i.e., the anatomy of axons is dynamic, although it is seen usually in its `normal' state. the occurrence of ribosomes and messenger rnas in the axon suggests that axoplasmic proteins are most likely synthesized locally, at variance with the accepted notion that they are supplied by the cell body. we propose that the supporting cell (oligodendrocyte or schwann cell) regulates the axonal phenotype by fine-tuning the ongoing axonal protein synthesis.
Local regulation of the axonal phenotype, a case of merotrophism
Biological Research , 2005,
Abstract: In this essay, we show that several anatomical features of the axon, namely, microtubular content, caliber and extension of sprouts, correlate on a local basis with the particular condition of the glial cell, i.e., the anatomy of axons is dynamic, although it is seen usually in its `normal' state. The occurrence of ribosomes and messenger RNAs in the axon suggests that axoplasmic proteins are most likely synthesized locally, at variance with the accepted notion that they are supplied by the cell body. We propose that the supporting cell (oligodendrocyte or Schwann cell) regulates the axonal phenotype by fine-tuning the ongoing axonal protein synthesis.
A Gene Network Perspective on Axonal Regeneration
Ronald E. van Kesteren,Matthew R. J. Mason,Harold D. MacGillavry,August B. Smit,Joost Verhaagen
Frontiers in Molecular Neuroscience , 2011, DOI: 10.3389/fnmol.2011.00046
Abstract: The regenerative capacity of injured neurons in the central nervous system is limited due to the absence of a robust neuron-intrinsic injury-induced gene response that supports axon regeneration. In peripheral neurons axotomy induces a large cohort of regeneration-associated genes (RAGs). The forced expression of some of these RAGs in injured neurons has some beneficial effect on axon regeneration, but the reported effects are rather small. Transcription factors (TFs) provide a promising class of RAGs. TFs are hubs in the regeneration-associated gene network, and potentially control the coordinate expression of many RAGs simultaneously. Here we discuss the use of combined experimental and computational methods to identify novel regeneration-associated TFs with a key role in initiating and maintaining the RAG-response in injured neurons. We propose that a relatively small number of hub TFs with multiple functional connections in the RAG network might provide attractive new targets for gene-based and/or pharmacological approaches to promote axon regeneration in the central nervous system.
Serum Response Factor Mediated Gene Activity in Physiological and Pathological Processes of Neuronal Motility
Bernd Kn?ll
Frontiers in Molecular Neuroscience , 2011, DOI: 10.3389/fnmol.2011.00049
Abstract: In recent years, the transcription factor serum response factor (SRF) was shown to contribute to various physiological processes linked to neuronal motility. The latter include cell migration, axon guidance, and, e.g., synapse function relying on cytoskeletal dynamics, neurite outgrowth, axonal and dendritic differentiation, growth cone motility, and neurite branching. SRF teams up with myocardin related transcription factors (MRTFs) and ternary complex factors (TCFs) to mediate cellular actin cytoskeletal dynamics and the immediate-early gene (IEG) response, a bona fide indicator of neuronal activation. Herein, I will discuss how SRF and cofactors might modulate physiological processes of neuronal motility. Further, potential mechanisms engaged by neurite growth promoting molecules and axon guidance cues to target SRF’s transcriptional machinery in physiological neuronal motility will be presented. Of note, altered cytoskeletal dynamics and rapid initiation of an IEG response are a hallmark of injured neurons in various neurological disorders. Thus, SRF and its MRTF and TCF cofactors might emerge as a novel trio modulating peripheral and central axon regeneration.
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