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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.
A variety of angiogenic factors such as vascular endothelial growth factor are known to be involved in the progression of diabetic nephropathy. Vasohibin-2 (VASH2) is a novel pro-angiogenic factor. Increased expression of VASH2 is associated with tumor angiogenesis and growth. We previously reported that homozygous Vash2 knockout mice showed lower urinary albumin excretion and milder glomerular damage after induction of diabetes compared to wild-type (WT) mice. Recently, VASH2 has been reported to possess a novel function, α-tubulin detyrosinating enzymatic activity. In this study, we generated Vash2 transgenic (V2Tg) mice that overexpresses VASH2 under the control of β-actin promoter, and examined the roles of increased VASH2 expression in the pathogenesis of diabetic nephropathy including the alteration of tubulin detyrosination in podocytes.
In 8-week-old male C57BL/6J background WT and V2Tg mice, diabetes was induced by intraperitoneal administration of 50 mg/kg streptozotocin for 5 consecutive days, and hyperglycemia was confirmed after 4 weeks. Mice were subdivided into non-diabetic WT, non-diabetic V2Tg, diabetic WT, and diabetic V2Tg (n=6 in each group). Kidneys were harvested after 20 weeks.
Compared to WT mice, renal Vash2 mRNA expression was markedly increased in V2Tg mice and immunoreactivity for VASH2 was mainly detected in podocytes and tubular epithelial cells. Immunostaining on the kidney revealed that detyrosinated α-tubulin (deY-tub) was highly expressed in podocytes in WT mice and increased only in distal nephron in V2Tg mice. After induction of diabetes, urinary albumin excretion was significantly increased in V2Tg mice compared to WT mice independent of blood pressure and blood glucose. In addition, glomerular nephrin-positive area was significantly decreased in diabetic V2Tg mice. In parallel of the more severe podocyte injury, glomerular deY-tub-positive area was significantly decreased in diabetic V2Tg mice compared to diabetic WT mice, suggesting that increased urinary albumin excretion in diabetic V2Tg mice was not ascribed to increased deY-tub expression in podocytes.
Although VASH2 acts as both intracellular detyrosinating enzyme and extracellular pro-angiogenic factor, the latter function may have more important role in diabetes-induced glomerular injury with albuminuria.
