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Dimitriadis, A.

Publications and source records attributed to Dimitriadis, A..

2 recordsLinked to original sources

Mouse precision-cut liver and kidney slices: an optimized ex vivo model for acute toxicity testing

As excretion organs, the kidneys and liver are exposed to high concentrations of potentially toxic substances. While animal models remain the gold standard for organ-specific toxicity testing, alternative ex vivo approaches are essential to align with the 3R principles (refinement, reduction, replacement). Precision-cut tissue slices (PCTS) retain native tissue architecture, cellular heterogeneity, the interplay of different cell types, and metabolic capacity, offering a promising link between in vitro and in vivo models. Here, we aimed to establish an optimized protocol for preparing and culturing precision-cut kidney and liver slices (PCKS and PCLS) from mice for use in substance-oriented toxicological tests. Key parameters - including slice thickness, media composition, oxygenation, glucose levels, and incubation time - were refined to maintain tissue viability and metabolic function. Five known toxins - acetaminophen, cyclosporin A, cisplatin, arsenic trioxide, and aristolochic acid I - were tested. While PCKS showed comparable sensitivity to established kidney cell lines, PCLS achieved IC50 values closely matching in vivo toxicity data. High reproducibility across different experimenters was achieved, highlighting the robustness of the model. In conclusion, this ex vivo system provides a valuable, reproducible, and ethically approved platform for acute nephrotoxicity and hepatotoxicity testing, supporting preclinical drug screening and potentially reducing reliance on animal experiments.

pharmacology and toxicology↗

Single-nuclei transcriptomics of mammalian prion diseases identifies dynamic gene signatures shared between species

Mammalian prion diseases are fatal and transmissible neurological conditions caused by the propagation of prions, self-replicating multimeric assemblies of misfolded forms of host cellular prion protein (PrP). The most common human form of the disease, sporadic Creutzfeldt-Jakob disease (sCJD), typically presents as a rapidly progressive dementia and has no effective treatments. Prion diseases are transmissible to laboratory rodents affording unprecedented opportunities to understand neurodegeneration in its evolving stages. Murine models are especially useful in prion research as they develop bona fide prion disease and recapitulate all biochemical and neuropathological hallmarks of human prion disease. Despite extensive studies investigating the changes in transcriptional profiles in prion diseases the mechanisms by which prion diseases induce cellular toxicity, including changes in gene expression profiles are yet to be fully characterized. This is at least in part because confounding effects related to brain cellular heterogeneity have not been resolved. Here, we took advantage of the recent developments in single-cell technologies and performed an unbiased whole-transcriptome single-nucleus transcriptomic analysis in prion disease.

neuroscience↗