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.
Epigenetic alterations, as long as other various factors, have been suggested to contribute to the pathogenesis of acute kidney injury (AKI)-to-chronic kidney disease (CKD) transition; however, the details of the mechanism remain unclear. Recently, it has been suggested that some of epigenetic alterations induced by environmental stimuli may remain as “epigenetic memory” even after the stimuli disappears and contribute to the pathogenesis of late-onset diseases. In this study, focusing on changes in chromatin accessibility, we clarified the presence of “epigenetic memory” induced by AKI that may contribute to the progression of CKD through transcriptional regulation.
We induced ischemia-reperfusion injury (IRI) in mice as a disease model of AKI-to-CKD transition. Then we isolated tubular epithelial cells (TECs) from mice with AKI 48 hours after IRI, mice with renal fibrosis 6 weeks after IRI, and sham mice. We performed RNA-seq and ATAC-seq on isolated TECs to identify genomic regions in which increase in chromatin accessibility induced by AKI persisted even in the CKD stage, and analyzed their epigenetic features and transcriptional function.
We identified a total of 229 DNA regions as common differential accessibility regions (DARs) whose chromatin accessibility was increased both 48 hours and 6 weeks after IRI compared to sham samples. These common DARs were suggested to be “persistent ATAC peaks” whose chromatin accessibility was increased during AKI and maintained until the chronic phase as “epigenetic memory”. Most of them were located in the distal regions, possibly acting as enhancers on nearby genes. We focused on one of these ATAC peaks located about 90-kb upstream of the Ptpn12 gene, whose expression was transiently increased during AKI and returned to baseline afterwards. The histone modification states evaluated by temporal chromatin immunoprecipitation assay suggested that this persistent ATAC peak was an originally histone H3 lysine 27 acetylation (H3K27ac)-negative inactive enhancer, turned to be H3K27ac-positive active enhancer through experiencing IRI, and maintained its enhancer activity even after AKI. In vitro study using human primary cultured TECs demonstrated that the PTPN12 gene showed an enhanced upregulation following repeated hypoxic stimulation mimicking AKI, suggesting that this may be due to the enhancer function of the persistent ATAC peak activated by the initial hypoxic stimulation. The Ptpn12 gene has been suggested to contribute to cellular damage caused by IRI and fibrosis in other organs, and therefore, this persistent ATAC peak may be involved in the pathogenesis of AKI-to-CKD transition by causing primed reactivation of the Ptpn12 gene in response to repeated ischemic stimulation after experiencing an initial AKI.
We identified a novel enhancer that is activated by AKI and maintains its accessibility thereafter, which may contribute to the pathophysiology of AKI-to-CKD transition by inducing primed reactivation of the Ptpn12 gene on recurrent AKI.
