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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.
In chronic kidney disease (CKD), the loss of normal tubular structures and their replacement by extracellular matrix lead to progressive renal dysfunction. Cellular Communication Network Factor 1 (CCN1) is a matricellular protein involved in cell migration, proliferation, and extracellular matrix production. We recently reported that CCN1 is markedly upregulated in injured proximal tubules during the early phase after acute kidney injury (AKI), where it promotes the recruitment of fibroblasts and inflammatory cells around injured tubules, thereby contributing to tissue fibrosis (iScience, 2025). While CCN1 secretion from injured tubules is transiently induced during the acute phase, persistent CCN1 expression is observed in fibrotic kidneys. However, the role of CCN1 derived from non-tubular sources in the kidney remains unclear. Therefore, we hypothesized that fibroblast-derived CCN1 contributes to renal fibrosis during the chronic phase following injury, and we investigated its functional role.
Renal fibrosis was induced by unilateral ureteral obstruction (UUO) in wild-type (WT) and proximal tubule–specific CCN1 knockout (Epi-CCN1-KO) mice. Tissue fibrosis and the temporal pattern of CCN1 expression were evaluated. In vitro, CCN1-deficient NRK-49F fibroblasts were generated using the CRISPR–Cas9 system. Their migratory and proliferative capacities, as well as the expression of fibrosis-related genes, were assessed. RNA sequencing (RNA-seq) was performed to explore underlying molecular mechanisms.
While renal CCN1 expression was diminished in Epi-CCN1-KO mice during the acute phase after injury, CCN1 levels increased during the late phase of UUO-induced fibrosis in both WT and Epi-CCN1-KO mice, suggesting that CCN1 was secreted from non-tubular cells, particularly fibroblasts. CCN1-KO NRK-49F cells exhibited impaired migration and proliferation. Under TGF-β stimulation, CCN1 deficiency reduced Acta2 expression, indicating that CCN1 suppresses the transition of NRK-49F cells into myofibroblasts. Conditioned medium from CCN1-KO NRK-49F cells also attenuated fibroblast migration, suggesting that secreted CCN1 from NRK-49F cells contributes to these phenotypes. Gene ontology (GO) analysis of RNA-seq data revealed that biological processes related to positive regulation of cell population proliferation and cell migration were downregulated in CCN1-deficient NRK-49F cells.
Fibroblast-derived CCN1 enhances cell migration and proliferation while suppressing differentiation into myofibroblasts. Experiments using conditioned medium suggest that these effects are mediated through an autocrine mechanism of fibroblast-secreted CCN1. In vivo, elevated CCN1 expression was observed in fibrotic kidney tissue, where it may promote fibroblast recruitment to fibrotic areas while simultaneously limiting excessive fibrosis.
