The Injured Nerve

2017 ◽  
pp. 14-23
Author(s):  
Philippe Rigoard
Keyword(s):  
Injured Nerve

scholarly journals Engineered Stem Cells Improve Neurogenic Bladder by Overexpressing SDF-1 in a Pelvic Nerve Injury Rat Model

2020 ◽  
Vol 29 ◽  
pp. 096368972090246 ◽  
Author(s):  
Guan Qun Zhu ◽  
Seung Hwan Jeon ◽  
Kyu Won Lee ◽  
Hyuk Jin Cho ◽  
U-Syn Ha ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Growth Factor ◽  
Neurogenic Bladder ◽  
Rat Model ◽  
Bladder Wall ◽  
Bladder Function ◽  
Pelvic Nerve ◽  
Injured Nerve

There is still a lack of sufficient research on the mechanism behind neurogenic bladder (NB) treatment. The aim of this study was to explore the effect of overexpressed stromal cell-derived factor-1 (SDF-1) secreted by engineered immortalized mesenchymal stem cells (imMSCs) on the NB. In this study, primary bone marrow mesenchymal stem cells (BM-MSCs) were transfected into immortalized upregulated SDF-1-engineered BM-MSCs (imMSCs/eSDF-1+) or immortalized normal SDF-1-engineered BM-MSCs (imMSCs/eSDF-1−). NB rats induced by bilateral pelvic nerve (PN) transection were treated with imMSCs/eSDF-1+, imMSCs/eSDF-1−, or sham. After a 4-week treatment, the bladder function was assessed by cystometry and voiding pattern analysis. The PN and bladder tissues were evaluated via immunostaining and western blotting analysis. We found that imMSCs/eSDF-1+ expressed higher levels of SDF-1 in vitro and in vivo. The treatment of imMSCs/eSDF-1+ improved NB and evidently stimulated the recovery of bladder wall in NB rats. The recovery of injured nerve was more effective in the NB+imMSCs/eSDF-1+ group than in other groups. High SDF-1 expression improved the levels of vascular endothelial growth factor and basic fibroblast growth factor. Apoptosis was decreased after imMSCs injection, and was detected rarely in the NB+imMSCs/eSDF-1+ group. Injection of imMSCs boosted the expression of neuronal nitric oxide synthase, p-AKT, and p-ERK in the NB+imMSCs/eSDF-1+ group than in other groups. Our findings demonstrated that overexpression of SDF-1 induced additional MSC homing to the injured tissue, which improved the NB by accelerating the restoration of injured nerve in a rat model.

scholarly journals Oxidized lipids and signaling pathways of G2A receptor involved in nerve injury induced neuropathic pain

2021 ◽  
Author(s):  
◽  
Tabea Osthues
Keyword(s):  
Neuropathic Pain ◽  
Signaling Pathways ◽  
Nerve Injury ◽  
Inflammatory Mediators ◽  
Pain Perception ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Transient Receptor Potential Vanilloid ◽  
Wild Type ◽  
Injured Nerve

Neuropathic pain, a form of chronic pain, is a steadily rising health problem due to health costs and increasing numbers of patients. Neuropathic pain conditions arise upon metabolic disorders, infections, chemotherapeutic treatment, trauma or nerve injury. Especially nerve injury induced neuropathic pain is characterized by spontaneous or ongoing pain due to neuroimmune interactions. Thereby, inflammatory mediators, released by the injured nerve, recruit to and activate immune cells at the site of injury. Those mediators further activate transient receptor potential vanilloid 1 (TRPV1), a known channel involved in pain perception, or bind to G-protein coupled receptors (GPCR) in peripheral nerve endings. The following activated second messenger signaling pathways lead to sensitization of TRPV1. One of those GPCRs is G2A. The overall aim of this thesis was to investigate the role of G2A in nerve-injury induced neuropathic pain. For this, the common mouse model of nerve-injury induced neuropathic pain, the spared-nerve injury, was used. As measurements with dynamic plantar aesthesiometer showed, G2A-deficiency leads to reduced mechanical hypersensitivity. Upon analysis with FACS, ELISA and Luminex a reduced number of macrophages and neutrophils at the injured nerve, as well as less inflammatory mediators (TNFα, IL-6, VEGF) in G2A-deficient animals was observed. In dorsal root ganglia (DRGs) there was only a reduced number of macrophages and less IL-12 observed in G2A-deficient animals. Additionally, in wild-type mice, G2A agonist 9-HODE was elevated at the injured nerve, as a LC-MS/MS analysis showed. To investigate the underlying pathways of G2A-9-HODE signaling, a proteom screen was performed. This screen revealed upregulation of multiple proteins involved in migration in wild-type macrophages. Additionally, Ca-Imaging and transwell migration assays showed that the G2A antagonist G2A11, had desensitizing effects on DRG neurons and inhibited macrophage migration. Overall, the results suggest that loss of G2A has dual effects. On the one hand loss of G2A is antinociceptive. On the other hand, G2A-deficiency leads to reduced inflammation, suggesting G2A as promising target in treatment of neuropathic pain. Here, an antagonist had inhibitory effects on the migration and the sensitization.

scholarly journals Vimentin-Dependent Spatial Translocation of an Activated MAP Kinase in Injured Nerve

Neuron ◽  
2005 ◽  
Vol 45 (5) ◽  
pp. 715-726 ◽  
Author(s):  
Eran Perlson ◽  
Shlomit Hanz ◽  
Keren Ben-Yaakov ◽  
Yael Segal-Ruder ◽  
Rony Seger ◽  
...  
Keyword(s):  
Map Kinase ◽  
Injured Nerve

Morphological Changes of the Distal Segment of the Injured Nerve

1993 ◽  
Vol 28 (3) ◽  
pp. 1293
Author(s):  
Moon Sang Chung ◽  
Sang Hoon Lee ◽  
Young In Lee ◽  
Ki Se Nam
Keyword(s):  
Morphological Changes ◽  
Distal Segment ◽  
Injured Nerve

scholarly journals Macrophages and Associated Ligands in the Aged Injured Nerve: A Defective Dynamic That Contributes to Reduced Axonal Regrowth

2020 ◽  
Vol 12 ◽  
Author(s):  
Jo Anne Stratton ◽  
Shane Eaton ◽  
Nicole L. Rosin ◽  
Sana Jawad ◽  
Alexandra Holmes ◽  
...  
Keyword(s):  
Injured Nerve ◽  
Axonal Regrowth

scholarly journals Practical considerations concerning the use of stem cells for peripheral nerve repair

2009 ◽  
Vol 26 (2) ◽  
pp. E2 ◽  
Author(s):  
Sarah Walsh ◽  
_ _ ◽  
Rajiv Midha
Keyword(s):  
Stem Cells ◽  
Peripheral Nerve ◽  
Schwann Cells ◽  
Nerve Injury ◽  
Cell Fate ◽  
Peripheral Nerves ◽  
Nerve Repair ◽  
Precursor Cells ◽  
Host Cells ◽  
Injured Nerve

In this review the authors intend to demonstrate the need for supplementing conventional repair of the injured nerve with alternative therapies, namely transplantation of stem or progenitor cells. Although peripheral nerves do exhibit the potential to regenerate axons and reinnervate the end organ, outcome following severe nerve injury, even after repair, remains relatively poor. This is likely because of the extensive injury zone that prevents axon outgrowth. Even if outgrowth does occur, a relatively slow growth rate of regeneration results in prolonged denervation of the distal nerve. Whereas denervated Schwann cells (SCs) are key players in the early regenerative success of peripheral nerves, protracted loss of axonal contact renders Schwann cells unreceptive for axonal regeneration. Given that denervated Schwann cells appear to become effete, one logical approach is to support the distal denervated nerve environment by replacing host cells with those derived exogenously. A number of different sources of stem/precursor cells are being explored for their potential application in the scenario of peripheral nerve injury. The most promising candidate, transplant cells are derived from easily accessible sources such as the skin, bone marrow, or adipose tissue, all of which have demonstrated the capacity to differentiate into Schwann cell–like cells. Although recent studies have shown that stem cells can act as promising and beneficial adjuncts to nerve repair, considerable optimization of these therapies will be required for their potential to be realized in a clinical setting. The authors investigate the relevance of the delivery method (both the number and differentiation state of cells) on experimental outcomes, and seek to clarify whether stem cells must survive and differentiate in the injured nerve to convey a therapeutic effect. As our laboratory uses skin-derived precursor cells (SKPCs) in various nerve injury paradigms, we relate our findings on cell fate to other published studies to demonstrate the need to quantify stem cell survival and differentiation for future studies.

Opioids and TRPV1 in the peripheral control of neuropathic pain – Defining a target site in the injured nerve

2016 ◽  
Vol 101 ◽  
pp. 330-340 ◽  
Author(s):  
Dominika Labuz ◽  
Viola Spahn ◽  
Melih Özgür Celik ◽  
Halina Machelska
Keyword(s):  
Neuropathic Pain ◽  
Target Site ◽  
Injured Nerve
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