Peroxiredoxin 2 deletion impairs hippocampal-dependent memory via exacerbating transient ischemia-induced oxidative damage

Jang, Yoon-Sun; Lee, Yo-Seob; Kim, Dong‐Hee; Oh, Goo Taeg; Jeon, Won Kyung; Han, Jung‐Soo

doi:10.1016/j.brainresbull.2022.04.004

Cited by 2 publications

(3 citation statements)

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“…Low basal expression of PRXs along with the various modifications detected was suggested to contribute to the higher vulnerability of hippocampal neurons in neurodegenerative disorders [ 62 ]. Increased ROS can cause neuronal cell death in the CA1 of the hippocampus and its functional changes, such as learning and memory impairment [ 63 ]. Notably, oxidative and nitrosative changes, along with phosphorylation of PRXs, have been detected in the substantia nigra of Parkinson’s disease in both animal models and human subjects [ 62 , 64 ], resulting in deactivation of PRXs.…”

Section: Discussionmentioning

confidence: 99%

“…Notably, oxidative and nitrosative changes, along with phosphorylation of PRXs, have been detected in the substantia nigra of Parkinson’s disease in both animal models and human subjects [ 62 , 64 ], resulting in deactivation of PRXs. It was found that PRX2 deletion impairs hippocampal-dependent memory via aggravation of cerebral ischemia-induced oxidative damage in mice [ 63 ], while transgenic overexpression of PRX2 attenuated ischemic neuronal injury [ 65 ]. Injecting adenovirus-carrying PRX2 into the striatum a week before MPTP neurotoxic treatment notably prevented the loss of dopaminergic neurons in animals with Parkinson’s disease [ 64 ].…”

Section: Discussionmentioning

confidence: 99%

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Dynamics in Redox-Active Molecules Following Ischemic Preconditioning in the Brain

Lysikova,

Tomascova,

Kovalska

et al. 2024

Neurology International

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It is well known that the brain is quite vulnerable to oxidative stress, initiating neuronal loss after ischemia-reperfusion (IR) injury. A potent protective mechanism is ischemic preconditioning (IPC), where proteins are among the primary targets. This study explores redox-active proteins’ role in preserving energy supply. Adult rats were divided into the control, IR, and IPC groups. Protein profiling was conducted to identify modified proteins and then verified through activity assays, immunoblot, and immunohistochemical analyses. IPC protected cortex mitochondria, as evidenced by a 2.26-fold increase in superoxide dismutase (SOD) activity. Additionally, stable core subunits of respiratory chain complexes ensured sufficient energy production, supported by a 16.6% increase in ATP synthase activity. In hippocampal cells, IPC led to the downregulation of energy-related dehydrogenases, while a significantly higher level of peroxiredoxin 6 (PRX6) was observed. Notably, IPC significantly enhanced glutathione reductase activity to provide sufficient glutathione to maintain PRX6 function. Astrocytes may mobilize PRX6 to protect neurons during initial ischemic events, by decreased PRX6 positivity in astrocytes, accompanied by an increase in neurons following both IR injury and IPC. Maintained redox signaling via astrocyte-neuron communication triggers IPC’s protective state. The partnership among PRX6, SOD, and glutathione reductase appears essential in safeguarding and stabilizing the hippocampus.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Dynamics in Redox-Active Molecules Following Ischemic Preconditioning in the Brain

Lysikova,

Tomascova,

Kovalska

et al. 2024

Neurology International

View full text Add to dashboard Cite

show abstract

“…The essence of Prx2 is a peroxidase encoded by the Prdx2 gene [ 14 ], which has the effect of decomposing reactive oxygen species (ROS) [ 15 ]. In our earlier study, we determined the protective effect of Prx2 in animal experiments.…”

Section: Discussionmentioning

confidence: 99%

Peroxiredoxin 2 Is a Potential Objective Indicator for Severity and the Clinical Status of Subarachnoid Hemorrhage Patients

Peng

Pang

et al. 2023

Disease Markers

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Purpose. We have demonstrated that peroxiredoxin 2 (Prx2) released from lytic erythrocytes and damaged neurons into the subarachnoid space could activate microglia and then result in neuronal apoptosis. In this study, we tested the possibility of using Prx2 as an objective indicator for severity of the subarachnoid hemorrhage (SAH) and the clinical status of the patient. Materials and Methods. SAH patients were prospectively enrolled and followed up for 3 months. Cerebrospinal fluid (CSF) and blood samples were collected 0-3 and 5-7 days after SAH onset. The levels of Prx2 in the CSF and the blood were measured by an enzyme-linked immunosorbent assay (ELISA). We used Spearman’s rank coefficient to assess the correlation between Prx2 and the clinical scores. Receiver operating characteristic (ROC) curves were used for Prx2 levels to predict the outcome of SAH by calculating the area under the curve (AUC). Unpaired Student’s t -test was used to analyze the differences in continuous variables across cohorts. Results. Prx2 levels in the CSF increased after onset while those in the blood decreased. Existing data showed that Prx2 levels within 3 days in the CSF after SAH were positively correlated with the Hunt-Hess score ( R = 0.761 , P < 0.001 ). Patients with CVS had higher levels of Prx2 in their CSF within 5-7 days after onset. Prx2 levels in the CSF within 5-7 days can be used as a predictor of prognosis. The ratio of Prx2 in the CSF and the blood within 3 days of onset was positively correlated with the Hunt-Hess score and negatively correlated with Glasgow Outcome Scale (GOS; R = ‐ 0.605 , P < 0.05 ). Conclusion. We found that the levels of Prx2 in the CSF and the ratio of Prx2 in the CSF and the blood within 3 days of onset can be used as a biomarker to detect the severity of the disease and the clinical status of the patient.

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Peroxiredoxin 2 deletion impairs hippocampal-dependent memory via exacerbating transient ischemia-induced oxidative damage

Cited by 2 publications

References 40 publications

Dynamics in Redox-Active Molecules Following Ischemic Preconditioning in the Brain

Dynamics in Redox-Active Molecules Following Ischemic Preconditioning in the Brain

Peroxiredoxin 2 Is a Potential Objective Indicator for Severity and the Clinical Status of Subarachnoid Hemorrhage Patients

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