scholarly journals Extracellular Environment-Controlled Angiogenesis, and Potential Application for Peripheral Nerve Regeneration

2021 ◽  
Vol 22 (20) ◽  
pp. 11169
Author(s):  
Shingo Saio ◽  
Kanna Konishi ◽  
Hirofumi Hohjoh ◽  
Yuki Tamura ◽  
Teruaki Masutani ◽  
...  
Keyword(s):  
Peripheral Nerve ◽  
Nerve Regeneration ◽  
Molecular Mechanisms ◽  
Current Knowledge ◽  
Peripheral Nerve Regeneration ◽  
Review Article ◽  
Vascular Networks ◽  
Vascular Plexuses ◽  
Spatiotemporal Localization ◽  
Endothelial Growth Factor

Endothelial cells acquire different phenotypes to establish functional vascular networks. Vascular endothelial growth factor (VEGF) signaling induces endothelial proliferation, migration, and survival to regulate vascular development, which leads to the construction of a vascular plexuses with a regular morphology. The spatiotemporal localization of angiogenic factors and the extracellular matrix play fundamental roles in ensuring the proper regulation of angiogenesis. This review article highlights how and what kinds of extracellular environmental molecules regulate angiogenesis. Close interactions between the vascular and neural systems involve shared molecular mechanisms to coordinate developmental and regenerative processes. This review article focuses on current knowledge about the roles of angiogenesis in peripheral nerve regeneration and the latest therapeutic strategies for the treatment of peripheral nerve injury.

scholarly journals Therapeutic Low-Intensity Ultrasound for Peripheral Nerve Regeneration – A Schwann Cell Perspective

2022 ◽  
Vol 15 ◽  
Author(s):  
Jenica Acheta ◽  
Shannon B. Z. Stephens ◽  
Sophie Belin ◽  
Yannick Poitelon
Keyword(s):  
Peripheral Nerve ◽  
Nerve Regeneration ◽  
Schwann Cells ◽  
Nerve Injury ◽  
Peripheral Nerve Injury ◽  
Molecular Mechanisms ◽  
Peripheral Nerve Regeneration ◽  
Small Population ◽  
Low Intensity ◽  
Low Intensity Ultrasound

Peripheral nerve injuries are common conditions that can arise from trauma (e.g., compression, severance) and can lead to neuropathic pain as well as motor and sensory deficits. Although much knowledge exists on the mechanisms of injury and nerve regeneration, treatments that ensure functional recovery following peripheral nerve injury are limited. Schwann cells, the supporting glial cells in peripheral nerves, orchestrate the response to nerve injury, by converting to a “repair” phenotype. However, nerve regeneration is often suboptimal in humans as the repair Schwann cells do not sustain their repair phenotype long enough to support the prolonged regeneration times required for successful nerve regrowth. Thus, numerous strategies are currently focused on promoting and extending the Schwann cells repair phenotype. Low-intensity ultrasound (LIU) is a non-destructive therapeutic approach which has been shown to facilitate peripheral nerve regeneration following nerve injury in rodents. Still, clinical trials in humans are scarce and limited to small population sizes. The benefit of LIU on nerve regeneration could possibly be mediated through the repair Schwann cells. In this review, we discuss the known and possible molecular mechanisms activated in response to LIU in repair Schwann cells to draw support and attention to LIU as a compelling regenerative treatment for peripheral nerve injury.

scholarly journals Mechanisms of Schwann cell plasticity involved in peripheral nerve repair after injury

2020 ◽  
Vol 77 (20) ◽  
pp. 3977-3989 ◽  
Author(s):  
Gianluigi Nocera ◽  
Claire Jacob
Keyword(s):  
Peripheral Nerve ◽  
Nerve Regeneration ◽  
Molecular Mechanisms ◽  
De Novo ◽  
Nerve Repair ◽  
Peripheral Nerve Regeneration ◽  
Critical Feature ◽  
Axonal Regrowth ◽  
De Novo Genes ◽  
Dynamic Cell

Abstract The great plasticity of Schwann cells (SCs), the myelinating glia of the peripheral nervous system (PNS), is a critical feature in the context of peripheral nerve regeneration following traumatic injuries and peripheral neuropathies. After a nerve damage, SCs are rapidly activated by injury-induced signals and respond by entering the repair program. During the repair program, SCs undergo dynamic cell reprogramming and morphogenic changes aimed at promoting nerve regeneration and functional recovery. SCs convert into a repair phenotype, activate negative regulators of myelination and demyelinate the damaged nerve. Moreover, they express many genes typical of their immature state as well as numerous de-novo genes. These genes modulate and drive the regeneration process by promoting neuronal survival, damaged axon disintegration, myelin clearance, axonal regrowth and guidance to their former target, and by finally remyelinating the regenerated axon. Many signaling pathways, transcriptional regulators and epigenetic mechanisms regulate these events. In this review, we discuss the main steps of the repair program with a particular focus on the molecular mechanisms that regulate SC plasticity following peripheral nerve injury.

scholarly journals Exosomes and Their MicroRNA Cargo: New Players in Peripheral Nerve Regeneration

2018 ◽  
Vol 32 (9) ◽  
pp. 765-776 ◽  
Author(s):  
Liming Qing ◽  
Huanwen Chen ◽  
Juyu Tang ◽  
Xiaofeng Jia
Keyword(s):  
Peripheral Nerve ◽  
Nerve Regeneration ◽  
Current Knowledge ◽  
Peripheral Nerve Regeneration ◽  
Critical Role ◽  
Treatment Strategies ◽  
Clinical Problem ◽  
Peripheral Nerve Injuries ◽  
Vascular Regeneration ◽  
Major Clinical Problem

Peripheral nerve injury is a major clinical problem and often results in a poor functional recovery. Despite obvious clinical need, treatment strategies have been largely suboptimal. In the nervous system, exosomes, which are nanosized extracellular vesicles, play a critical role in mediating intercellular communication. More specifically, microRNA carried by exosomes are involved in various key processes such as nerve and vascular regeneration, and exosomes originating from Schwann cells, macrophages, and mesenchymal stem cells can promote peripheral nerve regeneration. In this review, the current knowledge of exosomes’ and their miRNA cargo’s role in peripheral nerve regeneration are summarized. The possible future roles of exosomes in therapy and the potential for microRNA-containing exosomes to treat peripheral nerve injuries are also discussed.

scholarly journals Coordinated changes in the expression of Wnt pathway genes following human and rat peripheral nerve injury

PLoS ONE ◽  
2021 ◽  
Vol 16 (4) ◽  
pp. e0249748
Author(s):  
Arie C. van Vliet ◽  
Jinhui Lee ◽  
Marlijn van der Poel ◽  
Matthew R. J. Mason ◽  
Jasprina N. Noordermeer ◽  
...  
Keyword(s):  
Peripheral Nerve ◽  
Nerve Regeneration ◽  
Nerve Injury ◽  
Molecular Mechanisms ◽  
Expression Profiles ◽  
Peripheral Nerve Regeneration ◽  
Gene Clusters ◽  
Nerve Lesion ◽  
Injured Nerve ◽  
Wnt Ligands

A human neuroma-in continuity (NIC), formed following a peripheral nerve lesion, impedes functional recovery. The molecular mechanisms that underlie the formation of a NIC are poorly understood. Here we show that the expression of multiple genes of the Wnt family, including Wnt5a, is changed in NIC tissue from patients that underwent reconstructive surgery. The role of Wnt ligands in NIC pathology and nerve regeneration is of interest because Wnt ligands are implicated in tissue regeneration, fibrosis, axon repulsion and guidance. The observations in NIC prompted us to investigate the expression of Wnt ligands in the injured rat sciatic nerve and in the dorsal root ganglia (DRG). In the injured nerve, four gene clusters were identified with temporal expression profiles corresponding to particular phases of the regeneration process. In the DRG up- and down regulation of certain Wnt receptors suggests that nerve injury has an impact on the responsiveness of injured sensory neurons to Wnt ligands in the nerve. Immunohistochemistry showed that Schwann cells in the NIC and in the injured nerve are the source of Wnt5a, whereas the Wnt5a receptor Ryk is expressed by axons traversing the NIC. Taken together, these observations suggest a central role for Wnt signalling in peripheral nerve regeneration.

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