• Molecules and Cells
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• v.40 no.1
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• pp.10-16
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• 2017

When peripheral axons are damaged, neuronal injury signaling pathways induce transcriptional changes that support axon regeneration and consequent functional recovery. The recent development of bioinformatics techniques has allowed for the identification of many of the regeneration-associated genes that are regulated by neural injury, yet it remains unclear how global changes in transcriptome are coordinated. In this article, we review recent studies on the epigenetic mechanisms orchestrating changes in gene expression in response to nerve injury. We highlight the importance of epigenetic mechanisms in discriminating efficient axon regeneration in the peripheral nervous system and very limited axon regrowth in the central nervous system and discuss the therapeutic potential of targeting epigenetic regulators to improve neural recovery.

• The Journal of Korean Physical Therapy
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• v.11 no.3
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• pp.133-140
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• 1999

Why does the CNS not regenerate after injury? The failure of axonal regeneration in the CNS after injury is not due to an inherent inability of these neurons to regrowth axon. Recently, an inhibitory substrate effect of CNS has been discovered which could be directly invoked in the lack of regeneration. The failure of axon regrowth in the CNS is crucially influenced by the presence of neurtie growth inhibitor NI35/250 and possibly also by molecules such as myelin associated glycoprotein(MAG) and chondroitin sulphate proteoglycans(CSPGs). The application of the monoclonal antibody IN-1, which efficinetly neutralizes the N135/250 inhibitory molecules. This new finding has a strong impact on the development of, a new neuroscienctific research directed to stimulate axonal regeneration. In this review summarize the current knowledge on the factors and molecules involved in the regeneration failure.

• Molecules and Cells
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• v.47 no.1
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• pp.100006.1-100006.10
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• 2024

Nitric oxide (NO) serves as an evolutionarily conserved signaling molecule that plays an important role in a wide variety of cellular processes. Extensive studies in Drosophila melanogaster have revealed that NO signaling is required for development, physiology, and stress responses in many different types of cells. In neuronal cells, multiple NO signaling pathways appear to operate in different combinations to regulate learning and memory formation, synaptic transmission, selective synaptic connections, axon degeneration, and axon regrowth. During organ development, elevated NO signaling suppresses cell cycle progression, whereas downregulated NO leads to an increase in larval body size via modulation of hormone signaling. The most striking feature of the Drosophila NO synthase is that various stressors, such as neuropeptides, aberrant proteins, hypoxia, bacterial infection, and mechanical injury, can activate Drosophila NO synthase, initially regulating cellular physiology to enable cells to survive. However, under severe stress or pathophysiological conditions, high levels of NO promote regulated cell death and the development of neurodegenerative diseases. In this review, I highlight and discuss the current understanding of molecular mechanisms by which NO signaling regulates distinct cellular functions and behaviors.

• The Journal of Korean Medicine
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• v.31 no.1
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• pp.93-111
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• 2010

Objectives: The present study was performed to evaluate the potential effects of Bupleuri radix (SH) on regenerative activities in the peripheral sciatic nerve after crushing injury in rats. Methods: Axonal regeneration after crush injury in rats was analyzed by immunofluorescence staining using anti-NF-200 antibody and retrograde tracing of DiI-axons. Changes in protein levels in the sciatic nerve axons and DRG tissue were analyzed by Western blot analysis and immunofluorescence staining. Effects of SH extract treatment on neurite outgrowth was examined by immunofluorescence staining for cultured DRG neurons. Results: Major findings on the effects of SH extract treatment on axonal regeneration are summarized as follows. 1. SH-mediated enhancement in axonal regeneration was identified by immuno- fluorescence straining of NF-200 protein and retrograde tracing of DiI-labeled axons. 2. Axonal GAP-43 protein levels were upregulated by SH not only in the injured axons but also in the DRG sensory neurons corresponding to sciatic sensory axons. 3. Phospho-Erk1/2 protein levels were increased in both injured axonal area and DRG sensory neurons by SH. Phospho-Erk1/2 was also found in non-neuronal cells in the injured axons. 4. SH elevated levels of Cdc2 protein produced in Schwann cells in the distal portions of injured sciatic nerves. 5. The neurite outgrowth of DRG sensory neurons in culture was augmented by SH, and these changes were positively associated with GAP-43 production levels in the DRG neurons. Conclusions: These data suggest that SH extract improves the regenerative responses of injured peripheral neurons, and thus may be useful for understanding molecular basis for the development of therapeutic strategies.

• Journal of Haehwa Medicine
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• v.14 no.2
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• pp.107-112
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• 2005

Peripheral axons in vertebrate animals can regenerate after nerve injury and accomplish its functional recovery. Numerous studies have revealed that diverse molecular factors are induced during axonal regeneration and their potential roles in axonal regeneration have been studied. Examples is N-CAM, L1, P0, nerve growth factors, GAP-43 and so forth. However, most of the studies on axonal regeneration have been primarily focused on axon fiber regrowth and elucidating molecular factors, and relatively less is known about functional recovery. Also, specific drugs or drug components used in the oriental medicine in relation to nerve fiber regeneration have not been known. And thus, in the present, a study on the effect of Samul-tang components and Samul-tang extracts to regeneration of peripheral axon fiber is underway by immunofluorescence staining. Therefore, this prior application of Samul-tang with documents consideration is reported with a plea for further investigation.

• Journal of Haehwa Medicine
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• v.15 no.2
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• pp.181-186
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• 2006

Peripheral axons in vertebrate animals can regenerate after nerve injury and accomplish its functional recovery. Numerous studies have revealed that diverse molecular factors are induced during axonal regeneration and their potential roles in axonal regeneration have been studied. Examples is N-CAM, L1, P0, nerve growth factors, GAP-43 and so forth. However, most of the studies on axonal regeneration have been primarily focused on axon fiber regrowth and elucidating molecular factors, and relatively less is known about functional recovery. Also, specific drugs or drug components used in the oriental medicine in relation to nerve fiber regeneration have not been known. And thus, in the present, a study on the effect of Yukmijihwang-tang components and Yukmijihwang-tang extracts to regeneration of peripheral axon fiber is underway by immunofluorescence staining. Therefore, this prior application of Yukmijihwang-tang with documents consideration is reported with a plea for further investigation.