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During the congress, E-Posters will be accessible to all participants on the congress website 24/7, as well as in the E-poster stations in the congress center.
Preparing your E-Poster
Please review the E-Poster format requirements carefully when preparing your E-Poster. Should your E-Poster not meet the mentioned requirements, it may not be displayed as described above.
E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
Please follow the instructions below to input your abstract title.
Abstract titles should be brief and reflect the content of the abstract.
Podocytes are highly specialized epithelial cells that maintain the glomerular filtration barrier through their intricate interdigitating foot processes. These processes interconnect with those of adjacent podocytes to form slit diaphragms that ensure selective permeability. When injured, foot process effacement occurs, leading to proteinuria and the progression of chronic kidney disease (CKD). Therefore, maintaining the structural integrity of foot processes is crucial for preserving glomerular function.Myosin-X (Myo10) is an unconventional actin-based motor protein known to regulate filopodia formation, intracellular transport, and cellular morphogenesis. However, its role in podocyte differentiation remains poorly understood. This study aimed to clarify the spatiotemporal expression pattern of Myo10 during glomerular development and to elucidate its functional involvement in the formation and maintenance of podocyte foot processes.
Kidneys were collected from Sprague–Dawley rats at postnatal day (P)0, P7, 4 weeks, and 8 weeks. The expression of Myo10 and nephrin during glomerular maturation was examined by immunofluorescence staining.In vitro, differentiated rat podocyte line C7 cells were transfected with mCherry-tagged wild-type Myo10 or a PH domain–deleted mutant (ΔPH). To promote process elongation, cells were treated with the ROCK inhibitor Y-27632 or the cAMP activator forskolin, and the subcellular localization of Myo10 was analyzed. Morphological changes were evaluated by fluorescence microscopy.
Myo10 expression was scarcely detectable in immature podocytes (P0–P7) but markedly increased at 4–8 weeks of age. In C7 cells, Myo10 was localized to the tips and branching points of cellular processes. Overexpression of wild-type Myo10 induced numerous dendritic-like extensions, whereas this effect was abolished in ΔPH mutants. Treatment with forskolin or Y-27632 enhanced process elongation, during which endogenous Myo10 accumulated at the distal ends and branching sites of extended processes.
Myo10 expression increases during podocyte maturation and plays a crucial role in the formation and maintenance of foot processes. Overexpression of Myo10 in cultured podocytes promoted process branching and elongation, while stimulation with forskolin or Y-27632 further enhanced these morphological changes. Myo10 predominantly localized to the tips, branching regions, and cell bodies of elongated processes, suggesting that it contributes to podocyte morphogenesis by regulating process outgrowth and branching.Understanding this mechanism provides new insight into how cytoskeletal remodeling sustains the glomerular filtration barrier and may offer potential therapeutic targets for glomerular diseases characterized by podocyte injury and foot process effacement.
