Thioredoxin 1 protects astrocytes from oxidative stress by maintaining peroxiredoxin activity

Wang, Mengfei; Zhu, Kunting; Zhang, Luyu; Li, Lingyu; Zhao, Jing

doi:10.3892/mmr.2016.4855

Cited by 14 publications

(5 citation statements)

References 32 publications

(28 reference statements)

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“…The AP-1 binding site within the SPATA12 core promoter (77–302 bp) encompasses the sequence 5′-TGAGTCA-3′, a core sequence in the AP-1 motif also known as the TPA responsive element (TRE) ( 22 ), is demonstrated in Fig. 4B .…”

Section: Resultsmentioning

confidence: 99%

Role and underlying mechanism of SPATA12 in oxidative damage

Liu

et al. 2018

Oncol Lett

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Spermatogenesis-associated gene 12 (SPATA12) functions as an inhibitor in spermatogenesis and tumorigenesis. Our previous study demonstrated that SPATA12 may be induced in tumor cells by ultraviolet (UV) C-mediated DNA damage, suggesting its importance in maintaining genomic integrity. In order to understand whether and how SPATA12 responds to oxidative damage, the present study established a cellular model of oxidative stress by detecting the effect of H2O2 on cell viability and intracellular superoxide dismutase activity, and the levels of glutathione and malondialdehyde (MDA). Quantitative polymerase chain reaction results demonstrated that H2O2 upregulated the expression of SPATA12, and a dual luciferase reporter gene assay indicated that transcription factor activator protein-1 (AP-1) was involved in the response of SPATA12 to oxidative stress. Through the exogenous expression of SPATA12, it was identified that SPATA12 decreased the level of reactive oxygen species and MDA, and also may reduce the degree of cellular oxidative damage and apoptosis induced by H2O2. In addition, resveratrol was demonstrated to increase the expression of SPATA12 by activating AP-1, and it may be used as a nontoxic activator of the SPATA12 gene. In conclusion, these results suggest that SPATA12 is upregulated by oxidative stress via AP-1, and that the exogenous expression of SPATA12 protects against H2O2-induced oxidative damage and apoptosis.

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Section: Resultsmentioning

confidence: 99%

Role and underlying mechanism of SPATA12 in oxidative damage

Liu

et al. 2018

Oncol Lett

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“…We showed that Tat-Trx1 protein transduced into HT-22 cells and markedly inhibited HT-22 cell death, ROS generation, and DNA fragmentation caused by oxidative stress. Recent studies have shown that knockdown of Trx1 can decrease astrocyte cell viability in an oxygen glucose deprivation/reperfusion (OGD/R)-induced cell model, suggesting that Trx1 can protect astrocyte cells from oxidative stress by exerting anti-oxidant effects ( Wang et al ., 2016 ). Overexpression of Trx1 protein can significantly protect against progressive β-cell failure in a T2DM animal model ( Stosic-Grujicic et al ., 2008 ).…”

Section: Discussionmentioning

confidence: 99%

Protective Role of Transduced Tat-Thioredoxin1 (Trx1) against Oxidative Stress-Induced Neuronal Cell Death via ASK1-MAPK Signal Pathway

Yeo

Eum

Yeo

et al. 2021

Biomol Ther (Seoul)

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Oxidative stress plays a crucial role in the development of neuronal disorders including brain ischemic injury. Thioredoxin 1 (Trx1), a 12 kDa oxidoreductase, has anti-oxidant and anti-apoptotic functions in various cells. It has been highly implicated in brain ischemic injury. However, the protective mechanism of Trx1 against hippocampal neuronal cell death is not identified yet. Using a cell permeable Tat-Trx1 protein, protective mechanism of Trx1 against hydrogen peroxide-induced cell death was examined using HT-22 cells and an ischemic animal model. Transduced Tat-Trx1 markedly inhibited intracellular ROS levels, DNA fragmentation, and cell death in H 2 O 2 -treatment HT-22 cells. Tat-Trx1 also significantly inhibited phosphorylation of ASK1 and MAPKs in signaling pathways of HT-22 cells. In addition, Tat-Trx1 regulated expression levels of Akt, NF-κB, and apoptosis related proteins. In an ischemia animal model, Tat-Trx1 markedly protected hippocampal neuronal cell death and reduced astrocytes and microglia activation. These findings indicate that transduced Tat-Trx1 might be a potential therapeutic agent for treating ischemic injury.

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“…Previous studies have revealed that LPS can induce high levels of ROS and that antioxidants play a beneficial role against LPS-induced inflammation (52,53). It has been reported that Trx1 can protect cells against damage caused by oxidative stress in various diseases due to its anti-oxidant function (21,(54)(55)(56). In the present study, cell permeable fusion protein Tat-Trx1 transduced into macrophages and drastically reduced LPS-induced ROS generation and DNA damage, suggesting that Tat-Trx1 could play a beneficial role in cell survival against LPS-induced damage.…”

Section: Discussionmentioning

confidence: 99%

Tat‑thioredoxin 1 reduces inflammation by inhibiting pro‑inflammatory cytokines and modulating MAPK signaling

et al. 2021

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Thioredoxin 1 (Trx1) serves a central role in redox homeostasis. It is involved in numerous other processes, including oxidative stress and apoptosis. However, to the best of our knowledge, the role of Trx1 in inflammation remains to be explored. The present study investigated the function and mechanism of cell permeable fused Tat-Trx1 protein in macrophages and a mouse model. Transduction levels of Tat-Trx1 were determined via western blotting. Cellular distribution of transduced Tat-Trx1 was determined by fluorescence microscopy. 2' ,7'-Dichlorofluorescein diacetate and TUNEL staining were performed to determine the production of reactive oxygen species and DNA fragmentation. Protein and gene expression were measured by western blotting and reverse transcription-quantitative PCR (RT-qPCR), respectively. Effects of skin inflammation were determined using hematoxylin and eosin staining, changes in ear weight and ear thickness, and RT-qPCR in ear edema animal models. Transduced Tat-Trx1 inhibited lipopolysaccharide-induced cytotoxicity and activation of NF-κB, MAPK and Akt. Additionally, Tat-Trx1 markedly reduced the production of inducible nitric oxide synthase, cyclooxygenase-2, IL-1β, IL-6 and TNF-α in macrophages.In a 12-O-tetradecanoylphorbol-13-acetate-induced mouse model, Tat-Trx1 reduced inflammatory damage by inhibiting inflammatory mediator and cytokine production. Collectively, these results demonstrated that Tat-Trx1 could exert anti-inflammatory effects by inhibiting the production of pro-inflammatory mediators and cytokines and by modulating MAPK signaling. Therefore, Tat-Trx1 may be a useful therapeutic agent for diseases induced by inflammatory damage.

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Thioredoxin 1 protects astrocytes from oxidative stress by maintaining peroxiredoxin activity

Cited by 14 publications

References 32 publications

Role and underlying mechanism of SPATA12 in oxidative damage

Role and underlying mechanism of SPATA12 in oxidative damage

Protective Role of Transduced Tat-Thioredoxin1 (Trx1) against Oxidative Stress-Induced Neuronal Cell Death via ASK1-MAPK Signal Pathway

Tat‑thioredoxin 1 reduces inflammation by inhibiting pro‑inflammatory cytokines and modulating MAPK signaling

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