ArticleJournal of cellular and molecular medicine2015
Tat-antioxidant 1 protects against stress-induced hippocampal HT-22 cells death and attenuate ischaemic insult in animal model.
Article in Journal of cellular and molecular medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed.
- Cuproptosis in inflammation and cancer: molecular mechanisms and therapeutic targets.Molecular cancer · 2026Review
- ATOX1 Promotes Hepatocellular Carcinoma Carcinogenesis via Activation of the c-Myb/PI3K/AKT Signaling Pathway.Journal of clinical and translational hepatology · 2025Article
- Unveiling the Cuproptosis in Colitis and Colitis-Related Carcinogenesis: A Multifaceted Player and Immune Moderator.Research (Washington, D.C.) · 2025Review
- Copper chaperone antioxidant 1: multiple roles and a potential therapeutic target.Journal of molecular medicine (Berlin, Germany) · 2023Review
- Tat-indoleamine 2,3-dioxygenase 1 elicits neuroprotective effects on ischemic injury.BMB reports · 2020Article
- Article
- Transduced Tat-aldose Reductase Protects Hippocampal Neuronal Cells against Oxidative Stress-induced Damage.Experimental neurobiology · 2019Article
- Phosphoglycerate Mutase 1 Promotes Cell Proliferation and Neuroblast Differentiation in the Dentate Gyrus by Facilitating the Phosphorylation of cAMP Response Element-Binding Protein.Neurochemical research · 2019Article
- Tat-ATOX1 inhibits inflammatory responses via regulation of MAPK and NF-κB pathways.BMB reports · 2018Article
- Atrial remodeling and metabolic dysfunction in idiopathic isolated fibrotic atrial cardiomyopathy.International journal of cardiology · 2018Article
- Neuroprotective Effects of Sigesbeckia pubescens Extract on Glutamate-Induced Oxidative Stress in HT22 Cells via Downregulation of MAPK/caspase-3 Pathways.Cellular and molecular neurobiology · 2018Article
- Short-term incubation of gabapentin or pregabalin does not affect chemically induced injury in neuronal cell models in vitro.Journal of pain research · 2018Article
- Ethanolic extract of Streblus asper leaves protects against glutamate-induced toxicity in HT22 hippocampal neuronal cells and extends lifespan of Caenorhabditis elegans.BMC complementary and alternative medicine · 2017Article
- Tat-protein disulfide-isomerase A3: a possible candidate for preventing ischemic damage in the spinal cord.Cell death & disease · 2017Article
- Neuroprotective Effect of 3-(Naphthalen-2-Yl(Propoxy)Methyl)Azetidine Hydrochloride on Brain Ischaemia/Reperfusion Injury.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2017Article
- Icariside II, a novel phosphodiesterase 5 inhibitor, protects against HJournal of cellular and molecular medicine · 2017Article
- The Role of Copper Chaperone Atox1 in Coupling Redox Homeostasis to Intracellular Copper Distribution.Antioxidants (Basel, Switzerland) · 2016Review
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Authors and funding
17 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oxidative stress-induced reactive oxygen species (ROS) are responsible for various neuronal diseases. Antioxidant 1 (Atox1) regulates copper homoeostasis and promotes cellular antioxidant defence against toxins generated by ROS. The roles of Atox1 protein in ischaemia, however, remain unclear. In this study, we generated a protein transduction domain fused Tat-Atox1 and examined the roles of Tat-Atox1 in oxidative stress-induced hippocampal HT-22 cell death and an ischaemic injury animal model. Tat-Atox1 effectively transduced into HT-22 cells and it protected cells against the effects of hydrogen peroxide (H2O2)-induced toxicity including increasing of ROS levels and DNA fragmentation. At the same time, Tat-Atox1 regulated cellular survival signalling such as p53, Bad/Bcl-2, Akt and mitogen-activate protein kinases (MAPKs). In the animal ischaemia model, transduced Tat-Atox1 protected against neuronal cell death in the hippocampal CA1 region. In addition, Tat-Atox1 significantly decreased the activation of astrocytes and microglia as well as lipid peroxidation in the CA1 region after ischaemic insult. Taken together, these results indicate that transduced Tat-Atox1 protects against oxidative stress-induced HT-22 cell death and against neuronal damage in animal ischaemia model. Therefore, we suggest that Tat-Atox1 has potential as a therapeutic agent for the treatment of oxidative stress-induced ischaemic damage.
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