Putative roles of soluble trophic factors in facial nerve regeneration, target reinnervation, and recovery of vibrissal whisking

Bendella, Habib; Rink, Svenja; Grosheva, Maria; Sarıkcıoğlu, Levent; Gordon, Tessa; Angelov, Doychin N.

doi:10.1016/j.expneurol.2017.10.029

Cited by 21 publications

(9 citation statements)

References 237 publications

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“…At present, the clinical treatment of facial nerve injury is not standardized, and further research is needed to improve the treatment effect. Clinical common medications include steroid hormones to relieve acute facial swelling [22], neurotrophic factors to stimulate the regeneration of neurons [23,24], and incobotulinumtoxin A to relax stiff muscles [25]. In addition, another common approach is the surgical intervention of the facial nerve through nerve repair, replacement, and transplantation [26].…”

Section: Discussionmentioning

confidence: 99%

DHI increases the proliferation and migration of Schwann cells through PI3K/AKT pathway and the expression of CXCL12 and GDNF to promote facial nerve function repair

Gao¹,

Sun²,

Sun³

et al. 2021

Preprint

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BackgroundDanhong injection (DHI) is a commonly used drug in the treatment of cardiovascular and cerebrovascular diseases, and its neuroprotective research has been fully confirmed. Schwann cells, as myelin forming cells of peripheral nerve, play an important role in the process of injury and repair. The purpose of this study was to explore the effect of DHI on Schwann cells and its role in facial nerve injury.MethodsRSC 96 Schwann cells were treated with different concentrations (0 –2%) of DHI for different time intervals (12 and 36 h). Effect of DHI on cell viability and migration were determined by CCK8 and Transwell assays. The levels of PI3K-Akt signaling related proteins were measured by western blotting analysis, and the effects of DHI on GDNF and CXCL12 using Western Blot, RT-qPCR, and ELISA assays at the cellular and animal levels, respectively. Then LY294002, an inhibitor of PI3K, was used to study the effect of DHI on cell migration and secretion of CXCL12 and GDNF in RSC96 cells by Transwell, Western Blot, RT-qPCR, and ELISA assays. Finally, facial nerve scoring and S-100 immunofluorescence staining were used to study the therapeutic effects of DHI on facial nerve injury.ResultsOur study found that DHI can promote the proliferation and migration of RSC96 cells, and this effect is related to the activation of PI3K/AKT pathway. LY294002 inhibits the proliferation and migration of RSC96 cells. Besides, DHI can also promote the expression of CXCL12 and GDNF at gene and protein levels, and CXCL12 is, while GDNF is not, PI3K/AKT pathway-dependent. Animal experiments confirmed that DHI could promote CXCL12 and GDNF expression, and promote facial nerve function recovery and myelin regeneration. Conclusion Our in vitro and in vivo experiments demonstrated that DHI could promote proliferation and migration of Schwann cells through the PI3K/AKT pathway, and increase the expression of CXCL12 and GDNF to promote facial nerve function repair.

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Section: Discussionmentioning

confidence: 99%

DHI increases the proliferation and migration of Schwann cells through PI3K/AKT pathway and the expression of CXCL12 and GDNF to promote facial nerve function repair

Gao¹,

Sun²,

Sun³

et al. 2021

Preprint

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“…It is also relevant to mention that successful NMJ regeneration is helped by signals derived from motor axon terminals and Schwann cells. For instance, nerve-released neurotrophic factors act as essential molecules to promote functional NMJ reinnervation (Bendella et al, 2018 ), whereas terminal Schwann cell-derived guidance molecules, such as CXCL12α, play essential roles in guiding motor axons to muscle fibers for functional repair (Negro et al, 2017 ). Also, recent findings reveal that local delivery of VEGF plus IGF-1, specifically at the distal site of sciatic nerve injury (i.e towards the NMJ), promoted functional reinnervation and muscle regeneration (Raimondo et al, 2019 ).…”

Section: Discussionmentioning

confidence: 99%

The Mouse Levator Auris Longus Muscle: An Amenable Model System to Study the Role of Postsynaptic Proteins to the Maintenance and Regeneration of the Neuromuscular Synapse

Ojeda

Bermedo‐García

Pérez

et al. 2020

Front. Cell. Neurosci.

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“…To prevent sarcopenia in aging, facilitation of muscle reinnervation is important. Several neurotrophins and cytokines are known to be involved in axon regeneration and sprouting, such as NGF, BDNF, IGF, and FGF2 (Bendella et al, ; English, ; Raivich & Makwana, ; Zhao, Veltri, Li, Bain, & Fahnestock, ). Since SC bridges and tubes are strong stimulant of axonal growth, further studies are essential to find ways of inducing or increasing factors released by SC or preventing SC's declining ability of producing trophic or tropic factors for facilitating axonal sprouts or growth.…”

Section: Discussionmentioning

confidence: 99%

“…Reinnervation via an escape fiber bridge from a nearby synaptic site can cause polyneuronal innervation of the same junction with an axon regenerated through original SC tube. Sustained polyinnervation of neuromuscular synapses can cause “postparalytic syndrome” and many nerve injury‐associated neurotrophic factors and cytokines, such as FGF2 and NGF, are timely regulated to prevent polyinnervation (Bendella et al, ; Grosheva et al, ).…”

Section: Discussionmentioning

confidence: 99%

Schwann cell guidance of nerve growth between synaptic sites explains changes in the pattern of muscle innervation and remodeling of synaptic sites following peripheral nerve injuries

Kang

Tian

Thompson

2019

J of Comparative Neurology

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Terminal Schwann cells (SCs) are nonmyelinating glia that are a prominent component of the neuromuscular junction (NMJ) where motor neurons form synapses onto muscle fibers. These cells play important roles not only in development and maintenance of the neuromuscular synapse but also restoring synaptic function after nerve damage. In response to muscle denervation, terminal SCs undergo dramatic changes in their gene expression patterns as well as in their morphology, such as extending elaborate processes into inter‐junctional space. These SC processes serve as a path to guide axon terminal sprouts from nearby innervated junctions, promoting rapid reinnervation of denervated fibers. We studied the role of terminal SCs in synapse reformation by using two different fluorescent proteins to simultaneously label motor axons and SCs; we examined these junctions repeatedly in living animals using a fluorescence microscope. Here, we show that alterations in the patterns of muscle innervation following recovery from nerve injury can be explained by SC guidance of regenerating axons. In turn, this guidance leads to remodeling of the NMJ itself.

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Putative roles of soluble trophic factors in facial nerve regeneration, target reinnervation, and recovery of vibrissal whisking

Cited by 21 publications

References 237 publications

DHI increases the proliferation and migration of Schwann cells through PI3K/AKT pathway and the expression of CXCL12 and GDNF to promote facial nerve function repair

DHI increases the proliferation and migration of Schwann cells through PI3K/AKT pathway and the expression of CXCL12 and GDNF to promote facial nerve function repair

The Mouse Levator Auris Longus Muscle: An Amenable Model System to Study the Role of Postsynaptic Proteins to the Maintenance and Regeneration of the Neuromuscular Synapse

Schwann cell guidance of nerve growth between synaptic sites explains changes in the pattern of muscle innervation and remodeling of synaptic sites following peripheral nerve injuries

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