Neural Organoids Protect Engineered Heart Tissues From Glucolipotoxicity by Transferring Versican in a Co-Culture System.

ABSTRACT: Metabolic disorders could cause dysregulated glucose and lipid at the systemic level, but how inter-tissue/organ communications contribute to glucolipotoxicity is difficult to dissect in animal models. To solve this problem, myocardium and nerve tissues were modelled by 3D engineered heart tissues (EHTs) and neural organoids (NOs), which were co-cultured in a generalised medium with normal or elevated glucose/fatty acid contents. Morphology, gene expression, cell death and functional assessments detected no apparent alterations of EHTs and NOs in co-culture under normal conditions. By contrast, NOs significantly ameliorated glucolipotoxicity in EHTs. Transcriptomic and protein secretion assays identified the extracellular matrix protein versican as a key molecule that was transferred from

SUBMITTER: Bai B 

PROVIDER: S-EPMC12774625 | biostudies-literature | 2026 Jan

REPOSITORIES: biostudies-literature