Changes of signaling molecules in the axotomized rat facial nucleus

Ishijima, Takashi; Nakajima, Kazuyuki

doi:10.1016/j.jchemneu.2022.102179

Cited by 7 publications

(11 citation statements)

References 33 publications

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“…However, the specific factors that induce and maintain microglia remain unknown. Following facial nerve transection, the CREB/ATF family is altered in neurons, and the phosphorylation of regulatory factors, such as CREB and JNK, is suppressed [ 17 ]. During this period, microglia, but not astrocytes, become activated, and the expression levels of CREB, ATF2, and p38 increase, all of which have been shown to play important roles in the central facial nerve.…”

Section: Discussionmentioning

confidence: 99%

Role of Facial Nerve Reconstruction With Anastomosis and Polyglycolic Acid Tube in Accelerating Functional Recovery After Axotomy in the Rat Facial Nucleus

Noda,

Koshu,

Takaso

et al. 2024

Cureus

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Facial nerve injuries stem from trauma or tumor surgery, triggering neurodegeneration and neuronal cell death in the facial nucleus, consequently inducing irreversible nerve paralysis. Following facial nerve transection, glial cells are activated and undergo proliferation, facilitating motor neuron survival, repair, and regeneration. Clinical approaches, including nerve anastomosis and hypoglossal nerve grafting, require delicate microscopic techniques. Recent advancements involve nerve reconstruction using polyglycolic acid (PGA) tubes, which yield nerve function improvement. However, the central pathophysiological effects of these procedures remain unclear. Therefore, using PGA tubes, we evaluated neurodegeneration and microglial inflammatory response in rats after facial nerve transection. Facial nerve functions were evaluated using vibrissae and blink reflex scores. In the end-to-end anastomosis and PGA tube reconstruction groups, a partial improvement in facial motor function was observed, with increased nerve fiber survival in the former. Approximately 90% of neurons survived in both groups, wherein gliosis exhibited increased microglial activation compared to that in the transection group. These results indicate that PGA tube-assisted nerve reconstruction post-facial nerve transection, although inferior to end-to-end anastomosis, improved certain functions and prevented neuronal cell death. Furthermore, the prolonged inflammatory response in the facial nerve nucleus underscored the correlation between neuronal function and survival and microglia.

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Section: Discussionmentioning

confidence: 99%

Role of Facial Nerve Reconstruction With Anastomosis and Polyglycolic Acid Tube in Accelerating Functional Recovery After Axotomy in the Rat Facial Nucleus

Noda,

Koshu,

Takaso

et al. 2024

Cureus

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“…In addition, it has been reported that cycloheximide alters protein degradation through activation of protein kinase B (PKB/AKT) [ 51 ], further enhancing NGB levels. On the other hand, resveratrol triggers the p38 activation, a well-known inducer of several transcription factors including CREB activation [ 52 , 53 , 54 ] that could overcome NRSF inhibition allowing Ngb transcription. Although Res stimulation prevents NGB degradation and enhances Ngb transcription, the contemporary treatment with cycloheximide reduces the NGB translation and the NGB protein overexpression could not occur.…”

Section: Discussionmentioning

confidence: 99%

A Novel Resveratrol-Induced Pathway Increases Neuron-Derived Cell Resilience against Oxidative Stress

Cracco

Montalesi

Parente

et al. 2023

IJMS

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A promising therapeutic strategy to delay and/or prevent the onset of neurodegenerative diseases (NDs) could be to restore neuroprotective pathways physiologically triggered by neurons against stress injury. Recently, we identified the accumulation of neuroglobin (NGB) in neuronal cells, induced by the 17β-estradiol (E2)/estrogen receptor β (ERβ) axis, as a protective response that increases mitochondria functionality and prevents the activation of apoptosis, increasing neuron resilience against oxidative stress. Here, we would verify if resveratrol (Res), an ERβ ligand, could reactivate NGB accumulation and its protective effects against oxidative stress in neuronal-derived cells (i.e., SH-SY5Y cells). Our results demonstrate that ERβ/NGB is a novel pathway triggered by low Res concentrations that lead to rapid and persistent NGB accumulation in the cytosol and in mitochondria, where the protein contributes to reducing the apoptotic death induced by hydrogen peroxide (H2O2). Intriguingly, Res conjugation with gold nanoparticles increases the stilbene efficacy in enhancing neuron resilience against oxidative stress. As a whole, ERβ/NGB axis regulation is a novel mechanism triggered by low concentration of Res to regulate, specifically, the neuronal cell resilience against oxidative stress reducing the triggering of the apoptotic cascade.

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“…Activation of ERK/CREB pathway is an important molecular mechanism for promoting nerve regeneration after nerve injury ( Jiao et al, 2005 ). it was discovered that downregulation of motoneuron-specific molecules was linked to the activation of the ERK/CREB pathway, which was crucial for the regeneration of motor neurons in rats with facial axonotomies ( Ishijima and Nakajima, 2022 ). Seo et al found that, ERK/CREB pathway was inhibited in the model rats with sciatic nerve injury, while exercise training and bone marrow stromal cell implantation could significantly activate ERK/CREB pathway and then promote nerve regeneration ( Seo et al, 2021 ).…”

Section: Adverse Effects Of Analgesics Related To Nervous Systemmentioning

confidence: 99%

Mechanism of ERK/CREB pathway in pain and analgesia

Zhen

Wang

et al. 2023

Front. Mol. Neurosci.

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Research has long centered on the pathophysiology of pain. The Transient Receiver Potential (TRP) protein family is well known for its function in the pathophysiology of pain, and extensive study has been done in this area. One of the significant mechanisms of pain etiology and analgesia that lacks a systematic synthesis and review is the ERK/CREB (Extracellular Signal-Regulated Kinase/CAMP Response Element Binding Protein) pathway. The ERK/CREB pathway-targeting analgesics may also cause a variety of adverse effects that call for specialized medical care. In this review, we systematically compiled the mechanism of the ERK/CREB pathway in the process of pain and analgesia, as well as the potential adverse effects on the nervous system brought on by the inhibition of the ERK/CREB pathway in analgesic drugs, and we suggested the corresponding solutions.

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Changes of signaling molecules in the axotomized rat facial nucleus

Cited by 7 publications

References 33 publications

Role of Facial Nerve Reconstruction With Anastomosis and Polyglycolic Acid Tube in Accelerating Functional Recovery After Axotomy in the Rat Facial Nucleus

Role of Facial Nerve Reconstruction With Anastomosis and Polyglycolic Acid Tube in Accelerating Functional Recovery After Axotomy in the Rat Facial Nucleus

A Novel Resveratrol-Induced Pathway Increases Neuron-Derived Cell Resilience against Oxidative Stress

Mechanism of ERK/CREB pathway in pain and analgesia

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