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Cell Proliferation

Cell Proliferation

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

Published:3 June 2025 DOI: 10.1111/cpr.70070 PMID: 40459298
Baochen Bai,?Jiting Li,?Ze Wang,?Yuhan Yang,?Jieqing He,?Gonglie Chen,?Yufan Zhang,?Yan Qi,?Zhongjun Wan,?Lin Cai,?Run Wang,?Kai Wang,?Dongyu Zhao,?Jingzhong Zhang,?Weihua Huang,?Ronald X Xu,?Mingzhai Sun,?Xiao Han,?Yan Liu,?Donghui Zhang,?Wanying Zhu,?Jian Liu,?Yuxuan Guo

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 NOs into EHTs in the high-glucose/fatty acid condition. Recombinant versican protein treatment was sufficient to reduce glucolipotoxicity in EHTs. Adeno-associated virus-delivered versican overexpression was sufficient to ameliorate cardiac dysfunction in a murine model of diabetic cardiomyopathy. These data provide the proof-of-concept evidence that inter-tissue/organ communications exist in the co-culture of engineered tissues and organoids, which could be systemically studied to explore potential pathological mechanisms and therapeutic strategies for multi-organ diseases in?vitro.

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