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Biology subjects

Abdalkader, R. K.

Publications and source records attributed to Abdalkader, R. K..

2 recordsLinked to original sources

Quick and robust method for the generation of human iPSC-derived choroid plexus organoids

The choroid plexus (ChP) is a key brain structure responsible for cerebrospinal fluid (CSF) production and forms a selective barrier that regulates brain homeostasis and immune surveillance. In vitro models of ChP are essential for studying CSF dynamics, viral entry, neuroinflammation, and CNS drug transport, yet current organoid protocols remain complex, slow, and difficult to reproduce. Here, we report a quick and robust method for the generation of human iPSC-derived ChP organoids that is xeno-free/ serum-free, scalable, and reproducible. Early GSK3{beta} inhibition and transient WNT modulation guide organoids toward cystic ChP-enriched structures, confirmed by ventricle-like morphology and expression of canonical markers (TTR, ZO-1). This minimal workflow enables rapid production of functional ChP-like organoids suitable for CSF physiology studies, barrier modeling, and translational neuroscience, providing an accessible platform for both basic and applied research.

bioengineering↗

Modeling dry eye with an air-liquid interface in corneal epithelium-on-a-chip

Dry eye syndrome (DES) is a complex ocular condition characterized by an unstable tear film and inadequate tear production, leading to tissue damage. Despite its common occurrence, there is currently no comprehensive in vitro model that accurately reproduce the cellular characteristics of DES. Here we modified a corneal epithelium-on-a-chip (CEpOC) model to recapitulate DES by subjecting HCE-T human corneal epithelial cells to an air-liquid (AL) interface stimulus. We then assessed the effects of AL stimulation both in the presence and absence of diclofenac (DCF). Transcriptomic analysis revealed distinct gene expression changes in response to AL and AL_DCF, affecting pathways related to development, epithelial structure, inflammation, and extracellular matrix remodeling. Both treatments upregulated PIEZO2, linked to corneal damage signaling, while downregulating OCLN, involved in cell-cell junctions. They increased the expression of inflammatory genes (e.g., IL6) and reduced mucin production genes (e.g., MUC16), reflecting dry eye characteristics. TGFB1, crucial for corneal wound healing, was slightly downregulated in AL_DCF, potentially affecting wound healing processes rather than reducing inflammation by DCF. Metabolomic analysis showed increased secretion of metabolites associated with cell damage and inflammation (e.g., methyl-2-oxovaleric acid, 3-methyl-2-oxobutanoic acid, lauroyl-carnitine) in response to AL and even more with AL_DCF, indicating a shift in cellular metabolism. This study showcases the utilization of AL stimulus within the CEpOC as a comprehensive approach to faithfully reproduce the cellular characteristics of DES.

bioengineering↗