ArticleFrontiers in molecular neuroscience2025
Brain microvascular endothelial cells differentiated from a Friedreich's Ataxia patient iPSC are deficient in tight junction protein expression and paracellularly permeable.
Article in Frontiers in molecular neuroscience, 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.
- Restoring brain barriers: an innovative approach for treating neurological disorders.Fluids and barriers of the CNS · 2025Review
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Abstract
Friedreich's Ataxia (FA) is a rare, inherited ataxia resulting from GAA triplet expansions in the first intron of the Frataxin (FXN) gene, which encodes a mitochondrial protein involved in the incorporation of iron into iron-sulfur clusters. We previously identified decreased levels of F-actin and tight junction (TJ) proteins, which coincided with paracellular permeability in an FXN shRNA-mediated knockdown immortalized human brain microvascular endothelial cell (BMVEC) model. This premise is underexplored in the FA literature, prompting us to confirm these findings using a patient-derived iPSC model. One line each of FA patient iPSCs and age- and sex-matched
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