ArticleMolecular neurobiology2025
Knockdown of DJ-1 Exacerbates Neuron Apoptosis Induced by TgCtwh3 through the NF-κB Pathway.
Article in Molecular neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- DJ-1 Protects Human Retinal Endothelial Cells From Diabetes-Related Conditions and Prevents Ischemic Damage in Mouse Retinal Capillaries.Investigative ophthalmology & visual science · 2025Article
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13 authors.
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Abstract
Mutations or loss of function of DJ-1 and Toxoplasma gondii (T. gondii) infection has been linked to neurodegenerative diseases, which are often caused by oxidative stress. However, the relationship between DJ-1 and T. gondii infection is not yet fully understood. Therefore, this study aimed to investigate the expression of DJ-1 in the hippocampus tissue of mice or in HT22 infected with T. gondii Chinese 1 genotype Wh3 strain (TgCtwh3) and the effect of DJ-1 knockdown on neuronal apoptosis induced by TgCtwh3 tachyzoite, as well as the underlying mechanism at the cellular and molecular level. Firstly, we detected DJ-1 protein expression and cell apoptosis in the hippocampal tissue of mice infected by TgCtwh3. Then, we examined DJ-1 expression and apoptosis in HT22 challenged with TgCtwh3. Finally, we evaluated the apoptosis in HT22 with DJ-1 knockdown which was infected with TgCtwh3 and assayed the expression of NF-κBp65 and p-NF-κBp65. Our results showed that DJ-1 expression was reduced and neurons underwent apoptosis in the hippocampus of mice infected with TgCtwh3 tachyzoites. Additionally, the knockdown of DJ-1 followed by infection with TgCtwh3 tachyzoites led to increased apoptosis in HT22 cells through the NF-κB signaling pathway. Therefore, this study suggests that DJ-1 is an important target for preventing apoptosis caused by T. gondii TgCtwh3.
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