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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.
Kidney transplantation is a curative therapy for end-stage disease but demand far exceeds donor supply. Although de novo construction of a whole kidney from pluripotent stem cells is promising, it remains technically challenging. We therefore pursued a pragmatic strategy: reusing fetal animal kidneys as living scaffolds by selectively depleting renal progenitors, then supplying human renal progenitors to build three-dimensional tissue. Previously, we achieved interspecies nephron formation by eliminating host Six2-positive nephron progenitor cells (NPCs) and Foxd1-positive stromal progenitor cells (SPCs) using a diphtheria-toxin–based Cre-loxP system followed by transplantation of rat progenitors. However, because diphtheria toxin is harmful to human cells, a human-compatible ablation system was required. We therefore adopted the inducible caspase-9 (iC9) system, which selectively ablates fetal renal progenitors without injuring human cells.
Building on our earlier system for selective ablation of Six2+ cells, we newly generated Foxd1-iC9 mice by CRISPR knock-in of iC9 and a Venus reporter at the Foxd1 locus, enabling selective elimination of Foxd1+ (stromal progenitor) cells. These mice were crossed with wild-type female mice to obtain heterozygous E13.5 metanephros. Cultured on transwell inserts, ex vivo removal was induced by daily administration of the apoptosis inducer AP20187 (which induces Caspase9 dimerization) and an adjuvant. On days 3-4, removal efficiency was assessed by immunostaining. To verify replacement potential, stromal progenitor cells were sorted from the fetal kidney of a GFP-expressing mouse and microinjected into the Foxd1-iC9 metanephros post-removal. After continuing organ culture on the transwell for 3-4 days, chimeric structure was evaluated by immunostaining.
Activation of iC9 induced rapid and localized stromal cell death within 24 hours, with a marked reduction in Foxd1-positive cells by 48 hours and near-complete disappearance by the end of the culture. Nephron progenitor cells and the ureteric buds, however, were preserved. Meanwhile, disintegration of the cap mesenchyme formed by Six2-positive cells was observed. Importantly, GFP-positive stromal progenitor cells injected into Foxd1-iC9 metanephros survived, aligned along preserved structures, and formed chimeric structures alongside native cells. These findings establish that this platform is not a pure removal system but a replaceable cell replacement-compatible model.
We developed a new human-compatible mouse model that uses the iC9 system for selective ablation of renal progenitors. Foxd1-lineage ablation removes stromal components without collateral damage to other tissues, converts fetal kidneys into regenerative scaffolds, and enables structural refilling by exogenous stromal progenitors. Going forward, we aim to implement dual ablation of Six2 and Foxd1 lineages with subsequent complementation, toward constructing chimeric kidneys capable of supporting human nephron formation.
