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Updated: Jun 23, 2025

Model of Ischemic Heart Disease and Video-Based Comparison of Cardiomyocyte Contraction Using hiPSC-Derived Cardiomyocytes

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Published on: May 5, 2020

3D Computational Modeling of Defective Early Endosome Distribution in Human iPSC-Based Cardiomyopathy Models.

Hafiza Nosheen Saleem^1,2, Nadezda Ignatyeva^1,2, Christiaan Stuut^3,4

¹Heart Research Center Goettingen, Department of Cardiology and Pneumology, University Medical Center Goettingen, Georg-August University of Goettingen, 37077 Goettingen, Germany.

|June 19, 2024

Summary

A new computational model quantifies early endosome distribution in cells. This method revealed abnormal vesicle clustering in dilated cardiomyopathy models, which was corrected by RhoA II treatment, improving cargo transport.

Keywords:

STED computational modelling dilated cardiomyopathy endosomes heart failure human iPSCs signal processing signal transduction

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Last Updated: Jun 23, 2025

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Published on: March 14, 2021

Area of Science:

Cell Biology
Biophysics
Computational Biology

Background:

Intracellular cargo delivery relies on vesicle transport, with clathrin-mediated endocytosis (CME) being a key route via early endosomes.
The dynamic nature of endosomes challenges quantitative analysis, necessitating advanced modeling approaches.
Dilated cardiomyopathy (DCM) models exhibit defective vesicle distribution due to impaired CME signaling.

Purpose of the Study:

To introduce a novel computational modeling approach for assessing endosome distributions.
To analyze early endosome distribution in induced pluripotent stem cell-derived cardiomyocytes (iPSC-CMs) with DCM-associated mutations.
To investigate the effect of RhoA II treatment on rescuing endosome distribution defects.

Main Methods:

Developed a 3D spherical computational model for endosome distribution analysis.
Utilized iPSC-CMs with TPM1-L185F and TnT-R141W mutations (MUT) and wild-type (WT) controls.
Employed 3D confocal and super-resolution STED microscopy to image EEA1-positive vesicles.

Main Results:

Identified a bi-modal segregation of early endosome populations in MUT iPSC-CMs compared to WT controls.
Observed plasma membrane-localized early endosomes in MUT iPSC-CMs, indicative of impaired CME.
Demonstrated reversion of bi-modal vesicle localization in RhoA II-treated MUT iPSC-CMs, indicating restored homogeneous distribution.

Conclusions:

The developed 3D spherical modeling approach effectively assesses early endosome distribution in cell-based disease models.
Abnormal early endosome distribution in DCM iPSC-CMs can be rescued by RhoA II treatment, restoring CME-dependent signaling.
This method offers new insights into endosome network dynamics in various physiological and pathological conditions.