Potential Involvement of Snail Members in Neuronal Survival and Astrocytic Migration during the Gecko Spinal Cord Regeneration

Shen, T F; Wang, Yingjie; Zhang, Qing; Bai, Xue; Wei, Sumei; Zhang, Xuejie; Wang, Wenjuan; Yuan, Ying; Liu, Yan; Liu, Mei; Gu, Xiaosong; Wang, Yongjun

doi:10.3389/fncel.2017.00113

Cited by 4 publications

(4 citation statements)

References 66 publications

(89 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Unlike mammals, regenerating organisms such as fish, amphibians, and reptiles are capable of spinal cord regeneration after injury [30][31][32][33][34][35]. Clearly, axonal regrowth in these non-mammals occurs in a permissive milieu without inhibitory extracellular matrix components, glial scarring, or excessive activation of inflammation [30,32].…”

Section: Introductionmentioning

confidence: 99%

SOCS3 Attenuates GM-CSF/IFN-γ-Mediated Inflammation During Spontaneous Spinal Cord Regeneration

Zhang

et al. 2020

Neurosci. Bull.

Self Cite

View full text Add to dashboard Cite

SOCS3, a feedback inhibitor of the JAK/STAT signal pathway, negatively regulates axonal regrowth and inflammation in the central nervous system (CNS). Here, we demonstrated a distinct role of SOCS3 in the injured spinal cord of the gecko following tail amputation. Severing the gecko spinal cord did not evoke an inflammatory cascade except for an injury-stimulated elevation of the granulocyte/macrophage colony-stimulating factor (GM-CSF) and interferon gamma (IFN-c) cytokines. Simultaneously, the expression of SOCS3 was upregulated in microglia, and unexpectedly not in neurons. Enforced expression of SOCS3 was sufficient to suppress the GM-CSF/IFN-c-driven inflammatory responses through its KIR domain by attenuating the activities of JAK1 and JAK2. SOCS3 was also linked to GM-CSF/IFN-c-induced crosstolerance. Transfection of adenovirus overexpressing SOCS3 in the injured cord resulted in a significant decrease of inflammatory cytokines. These results reveal a distinct role of SOCS3 in the regenerating spinal cord, and provide new hints for CNS repair in mammals.

show abstract

Section: Introductionmentioning

confidence: 99%

SOCS3 Attenuates GM-CSF/IFN-γ-Mediated Inflammation During Spontaneous Spinal Cord Regeneration

Zhang

et al. 2020

Neurosci. Bull.

Self Cite

View full text Add to dashboard Cite

show abstract

“…This seems to depend on the correct topographic localization of the neurons (Dunlop et al, 2000). In addition, radial glial cells show an absence of scarring, highlighting a high plasticity during regeneration especially of the spinal cord (Gu et al, 2015;Shen et al, 2017).…”

Section: Reptilesmentioning

confidence: 96%

Neuronal regeneration: Vertebrates comparative overview and new perspectives for neurodegenerative diseases

et al. 2021

View full text Add to dashboard Cite

The central nervous system (CNS) has a reduced capacity to regenerate, and neuronal loss is often irreversible and can cause functional impairments (Gurgo et al., 2002;Li and Chen, 2016). Specific areas of brain control different nervous functions (Gudiene and Burba, 2003). Chronic diseases represent more than 60% of deaths in the world. Lifestyle, environmental factors and genetic predisposition can increase their incidence (Alesci, Miller et al., 2021). Neurodegenerative disorders are characterized by the progressive loss of neuron populations and can be classified according to their clinical presentation: with extrapyramidal and pyramidal symptoms, and with cognitive or behavioural disorders (Dugger and Dickson, 2017). They afflict a high percentage of the world's population, with predominance of dementia, Huntington's disease, amyotrophic lateral sclerosis (ALS), Alzheimer's disease (AD) and Parkinson's disease (PD) (Gitler et al., 2017). The estimates about these syndromes showed that they are the second cause of death in 2016 (Feigin and Vos, 2019), and lots of studies confirm that the number of people affected by dementia will increase, and by 2040, there will be 81.1 million people affected by this pathology (Ferri et al., 2005). These pathologies are chronic (Walker, 2018), and there is not yet a definitive cure. Some treatments aiming to slow down the progression of the neurodegenerative diseases, relieve the pain of the patient, improve symptoms and extend sufferer autonomy and functionality (Moosmann and Behl, 2002). Among the cures evaluated to treat these disorders, there is neuronal regeneration. Regenerative therapies, which are mainly based on the principle of neuroplasticity, use stem cell transplantation to produce new neurons (Li and Chen, 2016). However, this therapy fails to generate large quantities of neurons; furthermore, some factors,

show abstract

“…We then turned to a GD-induced cell apoptosis model, which has been successfully established to potentiate the apoptosis of gecko astrocytes [32]. Following the culture of Gsn3 in a glucose-free medium for 24 h, the apoptotic cell number increased significantly, as evidenced by the TUNEL method (Fig.…”

Section: Enforced Expression Of Gsocs1 Protected Oligodendrocytes Against Glucose Deprivation-induced Apoptosismentioning

confidence: 99%

Suppressors of cytokine signaling 1 protein in a regenerative model of the Gekko japonicus spinal cord

Wang

Sun

et al. 2021

Journal of Integrative Neuroscience

View full text Add to dashboard Cite

Demyelination is one of the pathological outcomes that occur immediately following spinal cord injury. Protection of oligodendrocytes against death/apoptosis proves to be beneficial for the preservation of neurological functions. Suppressors of cytokine signaling 1 protein inhibit the harmful effects of several inflammatory cytokines on oligodendrocytes, but its roles in spinal cord injury (SCI) induced apoptosis of oligodendrocytes remain unclear. We cloned suppressors of cytokine signaling 1 cDNA from Gekko japonicus (Japanese gecko) and analyzed the protein structure revealing the conserved domains contained in other vertebrate suppressors of cytokine signaling 1 proteins. The gecko suppressors of cytokine signaling 1 protein expression were increased in the injured spinal cord following gecko tail amputation and displayed colocalization with oligodendrocytes. The enforced expression of gecko suppressors of cytokine signaling 1 by adenovirus in the Gsn3 gecko oligodendrocyte cell line demonstrated that gecko suppressors of cytokine signaling 1 significantly suppressed cell apoptosis-induced by glucose deprivation. Determination of apoptosis-related proteins revealed that gecko suppressors of cytokine signaling 1 was able to activate extracellular regulated protein kinases (ERK) and serine/threonine protein kinases (Akt). The results presented a distinct protective role of gecko suppressors of cytokine signaling 1 in the regenerative model of the spinal cord, which may provide new cues for central nervous system repair in mammals.

show abstract

Potential Involvement of Snail Members in Neuronal Survival and Astrocytic Migration during the Gecko Spinal Cord Regeneration

Cited by 4 publications

References 66 publications

SOCS3 Attenuates GM-CSF/IFN-γ-Mediated Inflammation During Spontaneous Spinal Cord Regeneration

SOCS3 Attenuates GM-CSF/IFN-γ-Mediated Inflammation During Spontaneous Spinal Cord Regeneration

Neuronal regeneration: Vertebrates comparative overview and new perspectives for neurodegenerative diseases

Suppressors of cytokine signaling 1 protein in a regenerative model of the Gekko japonicus spinal cord

Contact Info

Product

Resources

About