Up-regulation of TNF Receptor-associated Factor 7 after spinal cord injury in rats may have implication for neuronal apoptosis

De-sheng, XU; Zhao, Wei; Wang, Chengniu; Zhu, Hao; He, Mingqing; Zhu, Xiao Feng; Liu, Wei; Wang, Fei; Fan, Jiyang; Chu, Chen; Cui, Daoran; Cui, Zhiming

doi:10.1016/j.npep.2018.08.001

Cited by 6 publications

(4 citation statements)

References 29 publications

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“…114 Neuronal apoptosis is also closely related to regulatory proteins, such as the RNA-binding protein src-associated in mitosis (Sam68), IGFBP6, a member of the insulin-like growth factor-binding protein family, HS1-associated protein X-1 (HAX1) and TNF receptor-associated factor 7 (TRAF7). [115][116][117][118] Ferroptosis is a novel type of irondependent cell death, and it has a strong correlation with secondary injury after SCI. 119 The inhibition of ferroptosis could promote the recovery of neurological function by enhancing neuronal survival.…”

Section: Immune Responses At the Peri-injury Sitementioning

confidence: 99%

Spinal cord injury: molecular mechanisms and therapeutic interventions

Ren

et al. 2023

Sig Transduct Target Ther

124

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Spinal cord injury (SCI) remains a severe condition with an extremely high disability rate. The challenges of SCI repair include its complex pathological mechanisms and the difficulties of neural regeneration in the central nervous system. In the past few decades, researchers have attempted to completely elucidate the pathological mechanism of SCI and identify effective strategies to promote axon regeneration and neural circuit remodeling, but the results have not been ideal. Recently, new pathological mechanisms of SCI, especially the interactions between immune and neural cell responses, have been revealed by single-cell sequencing and spatial transcriptome analysis. With the development of bioactive materials and stem cells, more attention has been focused on forming intermediate neural networks to promote neural regeneration and neural circuit reconstruction than on promoting axonal regeneration in the corticospinal tract. Furthermore, technologies to control physical parameters such as electricity, magnetism and ultrasound have been constantly innovated and applied in neural cell fate regulation. Among these advanced novel strategies and technologies, stem cell therapy, biomaterial transplantation, and electromagnetic stimulation have entered into the stage of clinical trials, and some of them have already been applied in clinical treatment. In this review, we outline the overall epidemiology and pathophysiology of SCI, expound on the latest research progress related to neural regeneration and circuit reconstruction in detail, and propose future directions for SCI repair and clinical applications.

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Section: Immune Responses At the Peri-injury Sitementioning

confidence: 99%

Spinal cord injury: molecular mechanisms and therapeutic interventions

Ren

et al. 2023

Sig Transduct Target Ther

124

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“…TRAF7 is a crucial regulatory protein that regulates whether the NF-κB transcription factor is activated or repressed [ 140 ]. TRAF7 also suppresses ECs apoptosis by increasing unusual polyubiquitination of the cellular fas-associated death domain-like IL-1-converting enzyme inhibitory protein (c-FLIP) [ 141 ] and the caspase-3-dependent pathway [ 142 ]. MiR-126-3p improves cell survival and decreases the expression of Bax and caspase-3 in high-glucose-induced human retinal ECs via targeting IL-17A and activating the PI3K/Akt pathway [ 143 ].…”

Section: Mechanism Of Exercise-induced Mir-126 In Improving Cardiovas...mentioning

confidence: 99%

Roles of physical exercise-induced MiR-126 in cardiovascular health of type 2 diabetes

Liu

Wang

et al. 2022

Diabetol Metab Syndr

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Although physical activity is widely recommended for preventing and treating cardiovascular complications of type 2 diabetes mellitus (T2DM), the underlying mechanisms remain unknown. MicroRNA-126 (miR-126) is an angiogenetic regulator abundant in endothelial cells (ECs) and endothelial progenitor cells (EPCs). It is primarily involved in angiogenesis, inflammation and apoptosis for cardiovascular protection. According to recent studies, the levels of miR-126 in the myocardium and circulation are affected by exercise protocol. High-intensity interval training (HIIT) or moderate-and high-intensity aerobic exercise, whether acute or chronic, can increase circulating miR-126 in healthy adults. Chronic aerobic exercise can effectively rescue the reduction of myocardial and circulating miR-126 and vascular endothelial growth factor (VEGF) in diabetic mice against diabetic vascular injury. Resistance exercise can raise circulating VEGF levels, but it may have a little influence on circulating miR-126. The Several targets of miR-126 have been suggested for cardiovascular fitness, such as sprouty-related EVH1 domain-containing protein 1 (SPRED1), phosphoinositide-3-kinase regulatory subunit 2 (PIK3R2), vascular cell adhesion molecule 1 (VCAM1), high-mobility group box 1 (HMGB1), and tumor necrosis factor receptor-associated factor 7 (TRAF7). Here, we present a comprehensive review of the roles of miR-126 and its downstream proteins as exercise mechanisms, and propose that miR-126 can be applied as an exercise indicator for cardiovascular prescriptions and as a preventive or therapeutic target for cardiovascular complications in T2DM.

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“…Spinal cord injury (SCI) is a serious threat to human health, which includes primary and secondary injuries. 1,2 Neuronal apoptosis is an important component of secondary SCI and spinal nerve cell death after SCI is caused by apoptosis. [3][4][5] Studies in different SCI models have confirmed that neuronal apoptosis is widespread in secondary SCI.…”

Section: Introductionmentioning

confidence: 99%

“…Spinal cord injury (SCI) is a serious threat to human health, which includes primary and secondary injuries . Neuronal apoptosis is an important component of secondary SCI and spinal nerve cell death after SCI is caused by apoptosis .…”

Section: Introductionmentioning

confidence: 99%

Rhein lysinate improves motor function in rats with spinal cord injury via inhibiting p38 MAPK pathway

Hao

Wang

Daiping

et al. 2019

The Kaohsiung J of Med Scie

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The current study aims to investigate the effect of rhein lysinate (RHL) on neuromotor function in rats with spinal cord injury (SCI) and to explore the underlying mechanism. A total of 63 adult male SD rats were randomly divided into the sham group, SCI group and RHL group (SCI‐RHL group), with 21 rats in each group. Basso Beattie Bresnahan (BBB) scoring and the inclined plate test were used to evaluate the changes in motor function after SCI. Then, superoxide dismutase (SOD), glutathione peroxidase (GSH‐Px), and malondialdehyde (MDA) contents were quantified. Caspase‐3‐positive cells in spinal cord tissue were detected by immunohistochemical (IHC) staining, and protein expression was detected by Western blots. Here, our data showed that compared with the SCI group, the BBB score and inclined plate test score of the SCI‐RHL group were significantly higher than those of the SCI group 7 days after the RHL intervention. After 7 days of RHL treatment, the activities of SOD and GSH‐Px in the spinal cord increased significantly. At the same time, RHL reduced the MDA content in spinal cord tissue of SCI rats. Moreover, cleaved‐caspase‐3‐positive cells and apoptotic cells were significantly lower in the SCI‐RHL group than in the SCI group. More importantly, p38 mitogen‐activated protein kinase (p38 MAPK) was significantly decreased in the SCI‐RHL group compared with the SCI group. In summary, RHL can inhibit the activation of the p38 MAPK pathway after SCI, thereby reducing the apoptosis of spinal cord neurons and improving the neuromotor function of SCI rats.

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Up-regulation of TNF Receptor-associated Factor 7 after spinal cord injury in rats may have implication for neuronal apoptosis

Cited by 6 publications

References 29 publications

Spinal cord injury: molecular mechanisms and therapeutic interventions

Spinal cord injury: molecular mechanisms and therapeutic interventions

Roles of physical exercise-induced MiR-126 in cardiovascular health of type 2 diabetes

Rhein lysinate improves motor function in rats with spinal cord injury via inhibiting p38 MAPK pathway

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