Tat-glyoxalase protein inhibits against ischemic neuronal cell damage and ameliorates ischemic injury

Shin, Min Jea; Kim, Dae Won; Lee, Yeom Pyo; Ahn, Eun Hee; Jo, Hyo Sang; Kim, Duk‐Soo; Kwon, Oh Nam; Kang, Tae‐Cheon; Cho, Yong‐Jun; Park, Jinseu; Eum, Won Sik; Choi, Soo Young

doi:10.1016/j.freeradbiomed.2013.10.815

Cited by 57 publications

(87 citation statements)

References 50 publications

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“…In a previous study, we demonstrated that PTD-antioxidant protein successfully transduced into astrocytes and significantly protected against oxidative stress-induced cell death in vitro and in vivo via its antioxidant role [19][20][21]. Moreover, we confirmed that several types of PTD fusion proteins have protective roles against cellular death in vivo and in vitro [22][23][24][25][26][27][28]. In this study, we demonstrate that Tat-PRAS40 protein significantly protects against oxidative stress-induced cellular death, suggesting that Tat-PRAS40 protein may be used as a therapeutic treatment for ischemia.…”

Section: Introductionsupporting

confidence: 59%

Tat-PRAS40 prevent hippocampal HT-22 cell death and oxidative stress induced animal brain ischemic insults

Shin

Kim

et al. 2016

Free Radical Biology and Medicine

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Section: Introductionsupporting

confidence: 59%

Tat-PRAS40 prevent hippocampal HT-22 cell death and oxidative stress induced animal brain ischemic insults

Shin

Kim

et al. 2016

Free Radical Biology and Medicine

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“…In previous studies, we demonstrated that transduced PTD fusion proteins protect against delayed pyramidal neuronal degeneration in the hippocampal CA1 region in an animal model of ischemia (23,33). Thus, the protective effects of Tat-NOL3 protein against ischemic damage were determined by immunohistochemistry.…”

Section: Discussionmentioning

confidence: 98%

“…To stain the nuclei, 1 µg/ ml DAPI (Roche Applied Science, Basel, Switzerland) was added for 2 min. Analysis was performed under a confocal fluorescence microscope (FA-300; Olympus, Tokyo, Japan) (23,30).…”

Section: Transduction Of Tat-nol3 Proteinmentioning

confidence: 99%

“…They were then exposed to biotinylated rabbit anti-goat IgG (1:200; Vector Laboratories, Inc., Burlingame, CA, USA) or goat antimouse IgG and streptavidin-peroxidase complex and visualized with 3,3'-diaminobenzidine (Sigma-Aldrich, St. Louis, MO, USA). Cresyl violet (CV; Junsei Chemical Co. Ltd., Saitama, Japan) and Fluoro-Jade B (FJB; Millipore Co., Temecula, CA, USA) staining were performed as previously described (23,33). Additionally, we performed immunostaining with a rabbit anti-histidine antibody and DAPI to detect the transduction of Tat-NOL3 protein in the brain hippocampus.…”

Section: Establishment Of An Animal Model Of Forebrain Ischemiamentioning

confidence: 99%

“…Many studies, including those conducted by our group have demonstrated that the Tat fusion proteins efficiently transduce into cells/tissues where they protect against various types of oxidative stress-induced cell death including neuronal cell death (16)(17)(18)(19)(20)(21)(22)(23)(24)(25).…”

Section: Introductionmentioning

confidence: 99%

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Tat-NOL3 protects against hippocampal neuronal cell death induced by oxidative stress through the regulation of apoptotic pathways

Sohn

Shin

Eum

et al. 2016

International Journal of Molecular Medicine

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Abstract. Oxidative stress-induced apoptosis is associated with neuronal cell death and ischemia. The NOL3 [nucleolar protein 3 (apoptosis repressor with CARD domain)] protein protects against oxidative stress-induced cell death. However, the protective mechanism responsible for this effect as well as the effects of NOL3 against oxidative stress in ischemia remain unclear. Thus, we examined the protective effects of NOL3 protein on hydrogen peroxide (H 2 O 2 )-induced oxidative stress and the mechanism responsible for these effects in hippocampal neuronal HT22 cells and in an animal model of forebrain ischemia using Tat-fused NOL3 protein (Tat-NOL3). Purified Tat-NOL3 protein transduced into the H 2 O 2 -exposed HT22 cells and inhibited the production of reactive oxygen species (ROS), DNA fragmentation and reduced mitochondrial membrane potential (Δ Ψm ). In addition, Tat-NOL3 prevented neuronal cell death through the regulation of apoptotic signaling pathways including Bax, Bcl-2, caspase-2, -3 and -8, PARP and p53. In addition, Tat-NOL3 protein transduced into the animal brains and significantly protected against neuronal cell death in the CA1 region of the hippocampus by regulating the activation of microglia and astrocytes. Taken together, these findings demonstrate that Tat-NOL3 protein protects against oxidative stress-induced neuronal cell death by regulating oxidative stress and by acting as an anti-apoptotic protein. Thus, we suggest that Tat-NOL3 represents a potential therapeutic agent for protection against ischemic brain injury.

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Lung–brain axis: Metabolomics and pathological changes in lungs and brain of respiratory syncytial virus‐infected mice

Mao

Bajinka

Tang

et al. 2022

Journal of Medical Virology

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The lung-brain axis is an emerging area of study that got its basis from the gut-brain axis biological pathway. Using Respiratory Synctial Virus (RSV) as the model of respiratory viral pathogen, this study aims to establish some biological pathways. After establishing the mice model, the inflammation in lung and brain were assayed using Hematoxylin-eosin staining, indirect immunofluorescence (IFA), and quantitative reverse-transcription polymerase chain reaction. The biological pathways between lung and brain were detected through metabolomics analysis. In lung, RSV infection promoted epithelial shedding and infiltration of inflammatory cells. Also, RSV immunofluorescence and titerss were significantly increased. Moreover, interleukin (IL)-1, IL-6 and tumor necrosis factor-α (TNF-α) were also significantly increased after RSV infection.In brain, the cell structure of hippocampal CA1 area was loose and disordered.Inflammatory cytokines IL-6 and IL-1β expression in the brain also increased, however, TNF-α expression showed no differences among the control and RSV group. We observed an increased expression of microglia biomarker IBA-1 and decreased neuronal biomarker NeuN. In addition, RSV mRNA expression levels were also increased in the brains. 15 metabolites were found upregulated in the RSV group including nerve-injuring metabolite glutaric acid, hydroxyglutaric acid and Spermine. ɑ-Estradiol increased significantly while normorphine decreased significantly at Day 7 of infection among the RSV group. This study established a mouse model for exploring the pathological changes in lungs and brains. There are many biological pathways between lung and brain, including direct translocation of RSV and metabolite pathway.

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Tat-glyoxalase protein inhibits against ischemic neuronal cell damage and ameliorates ischemic injury

Cited by 57 publications

References 50 publications

Tat-PRAS40 prevent hippocampal HT-22 cell death and oxidative stress induced animal brain ischemic insults

Tat-PRAS40 prevent hippocampal HT-22 cell death and oxidative stress induced animal brain ischemic insults

Tat-NOL3 protects against hippocampal neuronal cell death induced by oxidative stress through the regulation of apoptotic pathways

Lung–brain axis: Metabolomics and pathological changes in lungs and brain of respiratory syncytial virus‐infected mice

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