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.
Alport syndrome is a basement membrane disorder, characterized by hereditary nephropathy that results in irreversible, progressive renal failure. In the past decades, several Alport syndrome animal models have been produced in mice. The knockout mice for Col4α3, Col4α4, and Col4α5 have been developed and well characterized. The disease progression and pharmacological therapy were shown to genetic variability in the human patients. However, in spite of variabilities displayed in the genetic background, only a few mammalian models of Alport syndrome have been established.
We recently developed a novel method called Genome-editing via Oviductal Nucleic Acids Delivery (GONAD); a in vivo genome editing system that does not require ex vivo handling of embryos. In this study, we produced a novel Alport syndrome rat model using the rat GONAD technology, and investigated whether there are differences in the progression of glomerular disease among different rat strains.
Type IV Collagen α5 deficient rats were produced by the rGONAD method as previously described (Namba et al., Sci. Rep., 2021). All measurements of proteinuria, blood urea nitrogen (BUN), and serum creatinine (Cre) were performed according to the manufacturer’s recommended protocols.
We developed Col4α5 deficient mutant rats of the WKY, SD, DA, and F344 strains, identical to the Col4α5 G5X mutant mice. Col4α5 deficient rats exhibited hematuria, proteinuria, high levels of BUN, and CRE, and histological and ultrastructural analyses displayed the abnormalities including parietal cell hyperplasia, mesangial sclerosis, and interstitial fibrosis. Then, we demonstrated that α3/α4/α5 (IV) and α5/α5/α6 (IV) chains of type IV collagen were disrupted in the Col4α5 deficient rats. However, we found that there were strain-specific differences in the lifespan of the Col4α5 deficient rats. In the WKY rat strain, all hemizygous mutant males died from 18 to 28 weeks of age. In contrast, in the SD, DA and F344 rat strains, the lifespan of the hemizygous mutant males was much longer than that of the WKY males. To identify the QTL(s) affecting susceptibility to the lifespan in the Col4α5 deficient rats, we are currently examining the sequence differences in each rat's genome.
We first established the rat GONAD method for generating genome-edited rats, and described the generation of a novel rat model of Alport syndrome. Col4α5 deficient rats revealed typical physiological, pathological, and also histological characteristics of Alport syndrome. Moreover, we found that the progression of kidney disease in Aloprt rats differs depending on the rat strain. Thus, Col4α5 mutant rat is a reliable candidate for an Alport syndrome model animal for underlying the mechanism of renal diseases and further identifying potential therapeutic targets for human renal diseases.
