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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 (pro)renin receptor was initially identified as a receptor for renin and prorenin, and is now considered as a multifunctional protein involved in cellular homeostasis. In addition to mediating renin-angiotensin system activation, (pro)renin receptor contributes to vacuolar H+-ATPase function and Wnt signaling regulation. The full-length (pro)renin receptor undergoes post-translational cleavage by proteases including furin and site-1 protease (S1P) in the trans-Golgi network, generating two fragments: an N-terminal soluble form and a C-terminal transmembrane fragment. The physiological characteristics of these forms remain poorly understood. This study aimed to generate rats carrying mutation at the protease cleavage site of (pro)renin receptor using clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated protein 9 (Cas9)-based genome editing and to characterize the phenotypes of the cleavage site mutant rats.
Genome editing of the (pro)renin receptor cleavage site was performed in Sprague-Dawley rats using the rat genome-editing via oviductal nucleic acids delivery (rGONAD) technique, an in vivo CRISPR/Cas9-based mutagenesis method. At 8 weeks of age, blood pressure was measured in wild-type and mutant rats using the tail-cuff method, and the rats were euthanized. Biochemical, molecular and histological analyses were conducted.
Two types of gene-modified rats were obtained: a furin/S1P cleavage-site mutant and a furin cleavage-site deletion. Both gene-modified rats exhibited a complete absence of soluble (pro)renin receptor in plasma. Plasma renin activity and aldosterone concentration were decreased in both gene-modified rats compared with wild-type rats, while plasma total renin concentration, aldosterone-to-renin ratio, and blood pressure were not changed. Body weight was reduced in both gene-modified rats, although organ-to-body weight ratios of the kidney, heart, and brain, were comparable to those of wild-type rats. In the kidney, expression levels and staining patterns of (pro)renin receptor, renin-angiotensin components, and vacuolar H+-ATPase subunits were preserved.
Genetic modification of the (pro)renin receptor cleavage site abolished soluble (pro)renin receptor generation and resulted in reduced plasma renin activity and body weight without renal structural or molecular alterations. These findings suggest that soluble (pro)renin receptor may influence renin conformation or activity in plasma, and contribute to systemic body growth. Further studies are required to elucidate the physiological and pathophysiological roles of each (pro)renin receptor form.
