Method Profile
Previously injured kidney organoids are paired with cardiac microtissues to measure secondary viability, functional, vascular and expression changes.
Investigation of kidney-to-heart injury propagation and candidate mediators in a controlled human model.
Human iPSC-derived kidney organoids and cardiac microtissues containing cardiomyocytes, fibroblasts and endothelial cells.
Kidney injury induction followed by washing and static 72-hour co-culture; tissues are measured separately.
Human tissue systems
Kidney organoids and cardiac microtissues generated independently; doxorubicin and gentamicin produce distinct initiating injuries.
Measurements
ATP/LDH, 1 Hz-paced motion analysis, CD31/sarcomere staining and tissue-specific RNA sequencing.
Report the fraction of nonresponding cardiac tissues separately from contraction parameters calculated in pacing responders.
Compare cardiac tissues after co-culture with control, doxorubicin-injured or gentamicin-injured kidney organoids.
Limited stem-cell backgrounds; RNA comparisons used four biological replicates per tissue/condition, while imaging/function sampling varied by endpoint.
Control-kidney co-culture, separate cardiac culture and direct-drug reference experiments.
Doxorubicin-injured kidneys produced stronger cardiac viability, functional and endothelial changes; gentamicin had a weaker secondary effect.
Human kidney organoids were injured before co-culture with cardiac microtissues. Doxorubicin-injured kidneys produced stronger secondary cardiac changes than the gentamicin condition, with distinct effects on viability, contraction and endothelial structures.
