Back
For best output, select "Paper Size" as "A4" and "Margin" as "0" or "None".
To save or print to PDF, please select Print Destination > Save as PDF, enable Background Graphics under "More Settings", then click "Save".
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 constitute a critical component of the glomerular filtration barrier. Emerging evidence suggests striking parallels between the molecular machinery governing podocyte foot process architecture and dendritic morphogenesis. Rab11, a member of the Rab GTPase family, has been demonstrated to play essential roles in vesicle trafficking, membrane recycling, and dendritic arborization in neurons. However, the functional significance of Rab11 isoforms in podocyte biology and glomerular integrity remains poorly understood. We hypothesized that Rab11 family proteins are crucial regulators of podocyte foot process formation and that functional redundancy among Rab11 isoforms may mask their individual contributions to maintaining the glomerular filtration barrier.
Primary podocytes were isolated from Nphs2Cre DTRflox mice and cultured to assess the expression profile of Rab11 isoforms (Rab11a, Rab11b, and Rab25) by real-time PCR. To investigate the functional roles of Rab11 isoforms in vivo, we generated knockout mouse models: podocyte-specific Rab11a knockout (Nphs2Cre Rab11afl/fl DTRflox: Rab11a-cKO), Rab11b conventional knockout (Rab11b−/−: Rab11b-KO), and podocyte-specific Rab11a/Rab11b double knockout mice (Nphs2Cre Rab11afl/fl Rab11b−/− DTRflox: Rab11a/11b-DKO). Blood, urine, and kidney samples were collected from these mice to evaluate proteinuria, renal function, and histopathological changes.
Quantitative PCR analysis revealed substantial expression of both Rab11a and Rab11b mRNAs in primary cultured podocytes, while Rab25 expression was negligible. Rab11a-cKO mice and Rab11b-KO mice developed only mild, non-progressive proteinuria without significant deterioration of renal function or histological evidence of glomerulosclerosis or interstitial fibrosis at 6 months of age. In contrast, Rab11a/11b-DKO mice manifested massive proteinuria as early as 2 weeks of age. By 4 weeks of age, Rab11a/11b-DKO mice exhibited progressive glomerulosclerosis and severe tubulointerstitial fibrosis. All Rab11a/11b-DKO mice died before 10 weeks of age. Immunofluorescence analysis of glomeruli from 10-day-old Rab11a/11b-DKO mice revealed profound disorganization of the slit diaphragm, with irregular and diminished nephrin staining patterns along the glomerular basement membrane. Scanning electron microscopy demonstrated dramatic alterations in foot process architecture, including extensive foot process effacement.
Our findings demonstrate that Rab11a and Rab11b exhibit functional redundancy and are collectively indispensable for maintaining podocyte foot process architecture and glomerular filtration barrier integrity. These results identify Rab11-mediated vesicle trafficking as a fundamental mechanism underlying podocyte structural maintenance and suggest that dysregulation of Rab11 function may contribute to the pathogenesis of proteinuric kidney diseases.
