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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.
Collectrin (Tmem27) is a homologue of angiotensin-converting enzyme 2 (ACE2) but lacks a catalytic domain. The two genes are located in close proximity on the X chromosome. Collectrin functions as a chaperone for amino acid transporters in the kidney. Previous studies have reported that collectrin-knockout mice exhibit aminoaciduria, hypertension, and enhanced salt sensitivity. Recently, we generated collectrin-knockout rats and observed an intriguing phenotype characterized by renal enlargement. In this study, we investigated the mechanisms by which collectrin deficiency leads to kidney enlargement.
We used two collectrin-knockout rat lines with deletions of either 220 bp or 330 bp in exon 1 and its surrounding genomic regions at the collectrin locus (referred to as 220 KO and 330 KO, respectively). Male studies were conducted using collectrin–/Y and collectrin+/Y rats, and female studies were performed using collectrin–/– and collectrin+/– rats. Urinary and plasma electrolyte levels and osmolality were measured, and urinary amino acid levels were analyzed. RNA sequencing was performed to assess gene expression profiles in the kidney.
At 5 and 21 weeks of age, male 220 KO rats showed a significant increase in kidney weight and pan-aminoaciduria. At 5 weeks of age, both male and female 330 KO rats also exhibited increased kidney weight and pan-aminoaciduria. Significant positive correlations were observed between kidney weight and urinary excretion of amino acids including serine, alanine, valine, and leucine, at 5 weeks of age. Loss of collectrin did not affect urinary and plasma levels of sodium, potassium, chloride, calcium, glucose, inorganic phosphorus, and osmolarity. To estimate cell size, we measured the maximum length of 1,000 tubular cells individually. No significant difference in the cell length was observed between male 220 KO and control rats at 5 weeks of age. In contrast, the number of tubular cells per unit area was significantly increased in 5-week-old male 220 KO rats. Immunohistochemistry revealed a significant increase in proliferating cell nuclear antigen (PCNA)-positive tubular cells in male 220 KO and in both male and female 330 KO rats at 5 weeks of age. RNA sequencing followed by enrichment analyses using significantly altered genes in the kidneys from 5-week-old 220 KO males (|log2FC| ≥ 1, Q-value ≤ 0.05) did not identify any known renal hypertrophy or hyperplasia pathways. However, fam111a, a PCNA-binding protein, showed more than a ten-fold increase in gene expression.
Renal enlargement caused by collectrin deficiency appears to result from increased cell proliferation in association with aminoaciduria. Further studies are needed to investigate the role of fam111a in renal cell proliferation and its association with collectrin and aminoaciduria.
