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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.
Graft dysfunction, frequently resulting from injury sustained during transplantation, remains a common complication in kidney transplants. Renal cell death is a major driver of this injury and dysfunction, with necroptosis—regulated by receptor-interacting protein kinase 1 (RIPK1)—emerging as a critical mechanism. Protein phosphatase 1 regulatory subunit 3G (PPP1R3G), known to interact with protein phosphatase 1γ (PP1γ) in modulating kinase activity, has an unclear role in RIPK1 activation and tubular cell death. This study explores the contribution of PPP1R3G to necroptosis during kidney transplantation and assesses the therapeutic potential of a novel sulfono-γ-AApeptide foldamer, PGB-1, designed to disrupt the PPP1R3G/PP1γ interaction to mitigate graft injury.
In vitro cellular I/R and in vivo KTX mouse model were used in this study. Primary proximal tubular cells (PTCs) from Ppp1r3g+/+ (WT) and Ppp1r3g−/− (KO) mice were cultured and cell I/R was induced through hypoxia/reoxygenation. Cell viability and death were analyzed using CellTiter-Glo assay and Annexin V-Cy3/ SYTOX green staining, respectively. The activation of necroptosis pathway and inflammation factors were determined by real-time PCR and Western blotting. For the in vivo model, syngeneic KTX was performed using same-sex mice in WT and KO groups (10-12 weeks). Kidney graft injury and function were evaluated by measuring plasma creatine and BUN levels, PAS staining and cell death (immunofluorescent staining) and GFR values. In male C57BL/6 mice, a newly designed sulfono-γ-AApeptide foldamer, PGB-1 (PP1 gamma binding 1), was administrated to donor kidneys (5 µM in University of Wisconsin solution) during cold storage. Syngeneic KTX was conducted after 3 hours of cold storage, and graft injury and function were assessed at 1- and 3-days post-transplantation.
We found that deleting PPP1R3G in PTCs significantly enhanced cell viability and reduced tubular cell death. This protective effect was associated with lower activation of necroptosis markers (p-RIP1, p-RIP3, and p-MLKL) and reduced expression of inflammatory factors. In the KTX, PPP1R3G deletion mitigated I/R-induced kidney graft injury, demonstrated by a 51% decrease in plasma creatinine (1.78±0.16 vs. 0.87±0.18 mg/dL, p<0.001, n=7) and a 55% improvement in GFR in KO mice. Histological analysis showed reduced activated MLKL (p-S345-MLKL) and lower TUNEL staining in KO mice than WT. Additionally, administering PGB-1 to donor kidneys significantly protected grafts from ischemic injury, reducing plasma creatinine by 65% compared to controls.
This study demonstrates, for the first time, that Ppp1r3g-mediated necroptosis plays a significant role in kidney graft injury during transplantation. Blocking the PPP1R3G/PP1γ interaction with PGB-1 effectively halts cell death signaling, highlighting its potential as a therapeutic approach for human KTX.
