Expression of SGTA correlates with neuronal apoptosis and reactive gliosis after spinal cord injury

Chen, Minhao; Xia, Xiaopeng; Zhu, Xiao Feng; Cao, Jianhua; De-sheng, XU; Ni, Yingjie; Liu, Yang; Yan, Shi; Cheng, Xinghai; Liu, Yonghua; Wang, Youhua

doi:10.1007/s00441-014-1946-1

Cited by 14 publications

(7 citation statements)

References 37 publications

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“…Here, ATN1 , that encodes atrophin 1, a conserved transcriptional co-repressor [ 24 ] and whose expansions have been associated with neurodegeneration [ 25 ], was a hub (Additional file 2 : Table S1a). SGTA encodes a small glutamine-rich tetratricopeptide repeat (TPR)-containing, alpha that might be involved in neuronal apoptotic processes [ 26 ]. CRKL encodes an oncogene and seems pleiotropic in physiologic signalling [ 27 ], whilst TLE3 is a transcriptional co-repressor.…”

Section: Resultsmentioning

confidence: 99%

Frontotemporal dementia: insights into the biological underpinnings of disease through gene co-expression network analysis

Ferrari

Forabosco

Vandrovcová

et al. 2016

Mol Neurodegeneration

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BackgroundIn frontotemporal dementia (FTD) there is a critical lack in the understanding of biological and molecular mechanisms involved in disease pathogenesis. The heterogeneous genetic features associated with FTD suggest that multiple disease-mechanisms are likely to contribute to the development of this neurodegenerative condition.We here present a systems biology approach with the scope of i) shedding light on the biological processes potentially implicated in the pathogenesis of FTD and ii) identifying novel potential risk factors for FTD. We performed a gene co-expression network analysis of microarray expression data from 101 individuals without neurodegenerative diseases to explore regional-specific co-expression patterns in the frontal and temporal cortices for 12 genes (MAPT, GRN, CHMP2B, CTSC, HLA-DRA, TMEM106B, C9orf72, VCP, UBQLN2, OPTN, TARDBP and FUS) associated with FTD and we then carried out gene set enrichment and pathway analyses, and investigated known protein-protein interactors (PPIs) of FTD-genes products.ResultsGene co-expression networks revealed that several FTD-genes (such as MAPT and GRN, CTSC and HLA-DRA, TMEM106B, and C9orf72, VCP, UBQLN2 and OPTN) were clustering in modules of relevance in the frontal and temporal cortices. Functional annotation and pathway analyses of such modules indicated enrichment for: i) DNA metabolism, i.e. transcription regulation, DNA protection and chromatin remodelling (MAPT and GRN modules); ii) immune and lysosomal processes (CTSC and HLA-DRA modules), and; iii) protein meta/catabolism (C9orf72, VCP, UBQLN2 and OPTN, and TMEM106B modules). PPI analysis supported the results of the functional annotation and pathway analyses.ConclusionsThis work further characterizes known FTD-genes and elaborates on their biological relevance to disease: not only do we indicate likely impacted regional-specific biological processes driven by FTD-genes containing modules, but also do we suggest novel potential risk factors among the FTD-genes interactors as targets for further mechanistic characterization in hypothesis driven cell biology work.Electronic supplementary materialThe online version of this article (doi:10.1186/s13024-016-0085-4) contains supplementary material, which is available to authorized users.

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Section: Resultsmentioning

confidence: 99%

Frontotemporal dementia: insights into the biological underpinnings of disease through gene co-expression network analysis

Ferrari

Forabosco

Vandrovcová

et al. 2016

Mol Neurodegeneration

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“…As a micromolecule and free radical, NO possesses various bioactivities, including vasodilatation, neural information transmission and cytotoxic effects ( 23 ). Excessive NO can induce cell apoptosis, which is characteristic of the secondary changes exhibited following TSCI ( 24 ). In the current study, administration of allicin significantly inhibited the promotion of iNOS protein expression in TSCI mice.…”

Section: Discussionmentioning

confidence: 99%

Allicin protects traumatic spinal cord injury through regulating the HSP70/Akt/iNOS pathway in mice

Wang

Ren

2016

Molecular Medicine Reports

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Allicin is a major component of garlic, extracted as an oily liquid. The present study was designed to investigate the beneficial effects of allicin on traumatic spinal cord injury (TSCI) in mice, and whether the effects are mediated via regulation of the heat shock protein 70 (HSP70), v-akt murine thymoma viral oncogene homolog 1 (Akt) and inducible nitric oxide synthase (iNOS) pathways. Adult BALB/c mice (30–40 g) received a laminectomy at the T9 vertebral level as a model of TSCI. In the present study, treatment of the TSCI mice with allicin significantly increased their Basso, Beattie and Bresnahan (BBB) scores (P<0.01) and reduced the spinal cord water content (P<0.01). This protective effect was associated with the inhibition of oxidative stress and inflammatory responses in TSCI mice. Western blot analysis demonstrated that allicin increased the protein levels of HSP70, increased the phosphorylation of Akt and reduced the iNOS protein expression levels in TSCI mice. Additionally, treatment with allicin significantly reduced the levels of ROS and enhanced the NADH levels in TSCI mice. Collectively, these data demonstrate that the effects of allicin on TSCI are mediated via regulation of the HSP70, Akt and iNOS pathways in mice.

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“…The initial trauma is followed by complex, poorly understood changes resulting in further destruction of the spinal cord tissue over a period of several months, and consequently loss of the neural function. The apoptosis of neurons is an important mechanism in the pathogenesis of SCI [2,3]; therefore, the major strategy is to reduce neuronal damage, inhibit apoptosis, and to control inflammatory responses for promoting spinal cord repair. In recent years, the regulatory role of autophagy in SCI has become a popular area of research.…”

Section: Introductionmentioning

confidence: 99%

Diosgenin Glucoside Protects against Spinal Cord Injury by Regulating Autophagy and Alleviating Apoptosis

Chen

Wang

Yang

et al. 2018

IJMS

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Spinal cord injury (SCI) is a severe traumatic lesion of central nervous system (CNS) with only a limited number of restorative therapeutic options. Diosgenin glucoside (DG), a major bioactive ingredient of Trillium tschonoskii Max., possesses neuroprotective effects through its antioxidant and anti-apoptotic functions. In this study, we investigated the therapeutic benefit and underlying mechanisms of DG treatment in SCI. We found that in Sprague-Dawley rats with traumatic SCI, the expressions of autophagy marker Light Chain 3 (LC3) and Beclin1 were decreased with concomitant accumulation of autophagy substrate protein p62 and ubiquitinated proteins, indicating an impaired autophagic activity. DG treatment, however, significantly attenuated p62 expression and upregulated the Rheb/mTOR signaling pathway (evidenced as Ras homolog enriched in brain) due to the downregulation of miR-155-3p. We also observed significantly less tissue injury and edema in the DG-treated group, leading to appreciable functional recovery compared to that of the control group. Overall, the observed neuroprotection afforded by DG treatment warrants further investigation on its therapeutic potential in SCI.

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Expression of SGTA correlates with neuronal apoptosis and reactive gliosis after spinal cord injury

Cited by 14 publications

References 37 publications

Frontotemporal dementia: insights into the biological underpinnings of disease through gene co-expression network analysis

Frontotemporal dementia: insights into the biological underpinnings of disease through gene co-expression network analysis

Allicin protects traumatic spinal cord injury through regulating the HSP70/Akt/iNOS pathway in mice

Diosgenin Glucoside Protects against Spinal Cord Injury by Regulating Autophagy and Alleviating Apoptosis

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