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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 endothelial glycocalyx (eGLX) is a gel-like coating on vascular endothelial cells, composed of proteoglycans, such as syndecans, with glycosaminoglycan side chains such as heparan sulphate. eGLX regulates microvascular permeability, preventing protein loss from the circulation. The GLX of glomerular endothelial cells (GEnCs) forms the first layer of the glomerular filtration barrier. In diabetes, eGLX degradation leads to proteinuria, a hallmark of nephropathy. Matrix metalloproteinases (MMPs) and heparanase (HPSE) contribute to this by cleaving syndecans and heparan sulphate respectively. We hypothesise that HPSE and MMP are co-regulated in GEnCs under normal and diabetic conditions, and that their interaction contributes to eGLX loss, offering potential therapeutic targets.
Human GEnCs were treated for 8 hours with HPSE or control media. MMP-2, -9, and -14 mRNA expression levels were measured by qPCR and total MMP-2, active MMP-9, and SDC-4 protein levels were measured by ELISA. HPSE knockdown (KD) and scramble (Scr) control GEnCs were treated with control or diabetic media, and the same parameters were assessed. Separately, MMP-2, -9 and -14 KD and Scr GEnCs were treated with HPSE or control media, and HPSE and MMP mRNA and SDC-4 protein levels were quantified.
HPSE treatment increased MMP-14 mRNA (1.2-fold, p<0.01) and active MMP-9 protein levels (2.5 fold, p<0.05), while HPSE-KD reduced MMP-2 mRNA and protein levels in both control and diabetic conditions (all p<0.01). HPSE treatment increased SDC-4 shedding by 2-fold (p<0.001), and this proportional effect persisted despite MMP-2,-9 or -14 KD, suggesting partial MMP independence. HPSE mRNA levels increased with MMP-2 KD (1.4-fold, p<0.0001) and MMP-14 KD (1.2 fold, p<0.05), indicating reciprocal regulation.
HPSE modulates MMP expression and promotes SDC-4 shedding in GEnCs, contributing to eGLX degradation. These findings reveal a complex regulatory network and targeting this may protect the eGLX and preserve glomerular function in diabetes.
