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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.
The glomerulus is composed of endothelial cells, mesangial cells, and podocytes, and its integrity depends on biomechanical cues such as blood and interstitial flow. Endothelial cells experience shear stress, whereas mesangial cells are influenced by interstitial fluid flow. Although crosstalk between these two cell types is thought to stabilize glomerular structure, the underlying mechanisms remain unclear. We established a three-dimensional (3D) culture system that recapitulates key microenvironmental features to test how endothelial cells and fluidic stimulation regulate mesangial cell behavior.
We generated a collagen I gel–based 3D co-culture in which mouse mesangial cells (MES13) were embedded within the gel, and a mouse microvascular endothelial cell line (MS-1) was seeded on the gel surface. MES13 monocultures served as controls. Fluidic stimulation was applied to model physiological shear and interstitial flow. Structural and molecular endpoints included hematoxylin–eosin, VE-cadherin, picrosirius red, Ki67, and cleaved caspase-3 staining, and immunoblotting for p38, phospho-p38, Akt, and phospho-Akt.
Fluidic stimulation enhanced proliferation in both mesangial and endothelial compartments, indicating activation by the physical microenvironment. However, mesangial proliferation was significantly attenuated in co-culture relative to monoculture. The fractions of Ki67-positive and cleaved caspase-3–positive mesangial cells were both reduced in co-culture, consistent with a shift toward a quiescent, homeostatic state. In mesangial lysates, phosphorylation of p38 and Akt was downregulated under co-culture conditions, implicating endothelial-derived signals in dampening intracellular stress and survival pathways.
We demonstrate that endothelial–mesangial interactions are essential for glomerular homeostasis, acting to restrain mesangial cell proliferation and inhibit apoptosis. We found this critical angiocrine signaling is mediated specifically through the inhibition of p38 and Akt phosphorylation. These mechanisms were elucidated using a novel 3D perfusion platform that recapitulates physiological flow, establishing a mechanistic basis for glomerular stability. This system thus provides a powerful and tractable model to dissect specific angiocrine effectors and to screen therapeutic interventions for mesangial proliferative disorders.
