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Maas, R. G. C.

Publications and source records attributed to Maas, R. G. C..

3 recordsLinked to original sources

CardioShift: Resolving cell-to-cell functional heterogeneity in hiPSC-derived cardiomyocytes from high-throughput single-cell imaging

High-content screening of human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) is widely used for disease modeling, yet standard pipelines rely on whole-well averages that obscure cell-to-cell heterogeneity. Moving from well-averages to single-cell analysis reveals hidden variations, but may introduce a pseudoreplication bias if cells are analysed as independent data points. We present CardioShift, an open-source bioimage informatics framework designed to map single-cell distributions by properly accounting for this nested variance structure. Applying this framework to 32,818 Ca2+ transients and 10,719 contractility-lipid profiles, we show that cell-to-cell variability represents the largest source of variance for most functional parameters, demonstrating how traditional well averages mask condition-dependent phenotypes. Furthermore, unsupervised clustering identifies condition-dependent shifts in functional subpopulations, including a distinct cellular state that accumulates lipids but maintains baseline contraction kinetics that was not detected using well- and single-cell averaging approaches. CardioShift provides a robust analytical approach to resolve hidden single-cell distributions.

cell biology↗

Hypoxia and TNF-alpha modulate extracellular vesicle release from human induced pluripotent stem cell-derived cardiomyocytes

Extracellular vesicles (EVs) have emerged as important mediators of intercellular communication in the heart under homeostatic and pathological conditions, such as myocardial infarction (MI). However, the basic mechanisms driving cardiomyocyte-derived EV (CM-EV) production following stress are poorly understood. In this study, we generated human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) that express NanoLuc-tetraspanin reporters. These modified hiPSC-CMs allow for robust quantification of CM-EV secretion from small numbers of cells without the need for time-consuming EV isolation techniques. We subjected these cells to a panel of small molecules to study their effect on CM-EV biogenesis and secretion under basal and stress-associated conditions. We observed that EV biogenesis is context-dependent in hiPSC-CMs. Nutrient starvation decreases CM-EV secretion while hypoxia increases the production of CM-EVs in a nSmase2-dependent manner. Moreover, the inflammatory cytokine TNF- increased CM-EV secretion through a process involving NLRP3 inflammasome activation and mTOR signaling. Here, we detailed for the first time the regulatory mechanisms of EV biogenesis in hiPSC-CMs upon MI-associated stressors.

cell biology↗

Transcriptional regulation profiling reveals disrupted lipid metabolism in failing hearts with a pathogenic phospholamban mutation

BackgroundThe R14del mutation in the phospholamban (PLN) gene is associated with various types of cardiomyopathies and increases the risk of developing life-threatening ventricular arrhythmias. In this study, we focused on a homogeneous Dutch founder cohort of genetic cardiomyopathy due to PLN R14del mutation and aimed to study the influence of epigenetic changes from a multi-dimensional perspective. ResultsUsing cardiac tissue of PLN R14del patients and donors, we identified differentially acetylated promoters and enhancers (H3K27ac ChIPseq), annotated enriched transcription factor (TF) binding motifs located in those regions, and identified differentially expressed genes (RNA-seq). In line with the fibrofatty replacement in PLN R14del hearts at the histological level, our integrative analysis detected the downregulation of key TF regulators in fatty acid oxidation (FAO) metabolisms and their downstream target in PLN R14del hearts as compared to controls. We further examined heart tissue using immunofluorescence staining (IF) and to confirm the mitochondrial lipid abnormalities in the PLN R14del hearts. Furthermore, we observed the accumulation and deformation of lipid droplets and a disrupted morphology of mitochondria, the key organelle where FAO takes place, in PLN R14del heart using transmission electron microscopy (TEM). ConclusionUsing multi-omics approaches, we successfully obtained a unique list of chromatin regions and genes, including TF-coding genes, which played important roles in the metabolism-related signalling in PLN R14del hearts.

genomics↗