Peroxiredoxin-3 attenuates traumatic neuronal injury through preservation of mitochondrial function
| Autor: | Wei Hu, Shuai Li, Yue-Lin Zhang, Xingbo Dang, Gang Wang |
|---|---|
| Rok vydání: | 2018 |
| Předmět: |
0301 basic medicine
Mitochondrial DNA Peroxiredoxin III Mitochondrion medicine.disease_cause DNA Mitochondrial Rats Sprague-Dawley 03 medical and health sciences Cellular and Molecular Neuroscience medicine Animals Cells Cultured Cerebral Cortex Neurons chemistry.chemical_classification Reactive oxygen species Cell Biology Mitochondria Rats PRDX3 Cell biology Oxidative Stress 030104 developmental biology chemistry Mitochondrial biogenesis Peroxiredoxin Oxidative stress |
| Zdroj: | Neurochemistry International. 114:120-126 |
| ISSN: | 0197-0186 |
| DOI: | 10.1016/j.neuint.2018.02.004 |
| Popis: | Peroxiredoxins (PRDXs) are a highly conserved family of thiol peroxidases that scavenge peroxides in cells. PRDX3 is one member of PRDXs localized in the mitochondria, and has been shown to be involved in antioxidant defense and redox signaling. In this study, we investigated the role of PRDX3 in neuronal trauma using a traumatic neuronal injury (TNI) model in primary cultured cortical neurons. We found that TNI significantly decreased the expression of PRDX3 at both mRNA and protein levels. Overexpression of PRDX3 by lentivirus (LV-PRDX3) transfection attenuated lactate dehydrogenase (LDH) release and neuronal apoptosis after TNI. The results of immunostaining showed that LV-PRDX3 transfection markedly reduced TNI-induced intracellular ROS production, protein radical formation and lipid peroxidation. In addition, overexpression of PRDX3 preserved mitochondrial membrane potential (MMP) levels and ATP generation, and inhibited mitochondrial cytochrome c release in TNI-injured neurons. The results of polymerase chain reaction (PCR) showed that PRDX3 overexpression also increased mitochondrial DNA (mtDNA) content and upregulated the expression of mitochondrial biogenesis-related factors. Taken together, our data demonstrate that PRDX3 protects against TNI insult by preserving mitochondrial function and mitochondrial biogenesis, and may have potential therapeutic value for traumatic brain injury (TBI). |
| Databáze: | OpenAIRE |
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