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Biology subjects

Moon, B.-U.

Publications and source records attributed to Moon, B.-U..

3 recordsLinked to original sources

Human knee osteoarthritis patient-specific cartilage-on-a-chip model captures donor differences to stressors and treatments

Knee Osteoarthritis (KOA) is a progressive whole-joint disease without approved disease modifying OA drugs (DMOADs). Effective treatments have been hindered by multiple layers of heterogeneity, including diverse disease etiology and patient-to-patient variability. Here, we present a scalable, KOA patient-derived (PD) cartilage-on-a-chip (CartChip) model integrating end-stage KOA cartilage tissue explants on a microengineered platform that, under mechanical overloading and hyperinflammatory stressors, mimics different KOA etiologies. These stressors drove distinct multivariable model features, including changes in a curated panel of anabolic and catabolic genes, extracellular matrix protein and soluble factors. Exploratory analysis of coordinated model readouts identified stressor-agnostic and -specific KOA disease signatures. Despite using KOA tissue, the model showed improvements to dexamethasone, a symptom-modifying, anti-inflammatory KOA treatment. The model responses to dexamethasone were dependent on both stressor and donor heterogeneity. Exploratory groupings of coordinated model readouts provided proof-of-concept for predicting categories of patient responsiveness to test therapeutics. Annotating patient data provided additional donor-dependent contexts for interpreting model responsiveness. PD-CartChip provides a powerful research platform to potentially surmount the donor and stressor heterogeneity barrier in developing DMOADs.

bioengineering↗

PiP-plex: A Particle-in-Particle System for Multiplexed Quantification of Secreted Proteins by Single Cells

Cell signaling is modulated by the secretion of various proteins, which can be used to infer a cells phenotype. However, these proteins cannot be readily detected in multiplex by commonly used methods at the single cell level. Here, we present PiP-plex, a particles-in-particle (PiPs) system comprising (i) fluorescence intensity barcoded microparticles (BMPs) co-entrapped with (ii) a single cell inside an alginate hydrogel particle for multiplex protein secretion analysis by confocal microscopy. We show that developed PiPs maintained >90 % cellular viability and allowed live cells retrieval. A seven-plex fluorescent barcoding and concomitant sandwich immunoassay in PiPs were implemented with limits of detection ranging from 0.8 pg mL-1 to 2 ng mL-1 depending on the protein. PiP-plex assays were benchmarked with bulk immunoassays and found to rival or outperform them. We applied PiP-plex to analyze protein secreted by THP-1 cells upon exposure to lipopolysaccharide and detected varying cell responses, with a significant increase in MIP-1, TNF- and IL-17A. Multivariate analysis revealed that the majority of stimulated cells secreted either MIP-1 or IL-17A, while other cytokines were typically co-secreted. Using PiP-plex, we analyzed [~]750 THP-1 cells, showcasing its potential for characterizing cells and cell-based therapeutics for cancer immunotherapies.

bioengineering↗

Human cardiac-fibrosis-on-a-chip model recapitulates disease hallmarks and can serve as a platform for drug screening

While interstitial fibrosis plays a significant role in heart failure, our understanding of disease progression in humans is limited. To address this limitation, we have engineered a cardiac-fibrosis-on-a-chip model consisting of a microfabricated device with live force measurement capabilities using co-cultured human cardiac fibroblasts and pluripotent stem cell-derived cardiomyocytes. Transforming growth factor-{beta} was used as a trigger for fibrosis. Here, we have reproduced the classic hallmarks of fibrosis-induced heart failure including high collagen deposition, increased tissue stiffness, BNP secretion, and passive tension. Force of contraction was significantly decreased in fibrotic tissues that displayed a transcriptomic signature consistent with human cardiac fibrosis/heart failure. Treatment with an anti-fibrotic drug decreased tissue stiffness and BNP secretion, with corresponding changes in the transcriptomic signature. This model represents an accessible approach to study human heart failure in vitro, and allows for testing anti-fibrotic drugs while facilitating the real-time assessment of cardiomyocyte function.

bioengineering↗