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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.
Introduction: Diabetic kidney disease (DKD) is the most common cause of end stage renal disease globally and its pathogenesis continues to be unraveled. Recent studies underscore the role of Wnt-β catenin pathway (WBCP) in the DKD (Prabhakar et al, J Invest Med 2017). Epithelial mesenchymal transition (EMT) has been incriminated in the pathogenesis of DKD especially as a precursor to renal fibrosis. An RNAseq from the kidneys of adult ZSF1 obese vs. lean rats indicated Wnt9b as one of the most differentially expressed genes in ZSF1 obese (a log2fold of -11.45). We aimed to find the relationship between Wnt9b (aka Wnt14b) and EMT/mesenchymal to epithelial transition (MET) in the diabetic kidney. We evaluated the role of WBCP in EMT in DKD - both in experimental animal and cell culture models.
In vitro studies were conducted using cultured murine proximal tubular cells (TKPTS) and rat mesangial cells (RMC) in LG or low glucose (5.5mM) and HG or high glucose (25 mM) These cells were exposed to TGF-β to induce EMT. In vivo studies were performed in kidney homogenates from ZSF1 rats (male and female) euthanized at about 54 weeks of life. ZSF1 rats are a hybrid of ZDF (Zucker diabetic fatty) and spontaneously hypertensive heart-failure (SHHF) model rats and regarded as the best animal model to replicate human DKD. CD rats were used as controls TGF-β, Cadherins, Wnt9b and Tenascin C levels were assessed in these cellular and kidney homogenates using Western blot technique.
In the TKPTS cells in HG, (as opposed to in LG) TGF- expression was increased and TGF- β induced EMT was observed as evidenced by loose junctions and is associated with increased expression of Wnt9b and β-Catenin levels. In RMC, HG induced increased TGF- β expression compared to LG. HG decreased the expression of E-cadherin levels in TKPTS cells compared to LG. In the kidney homogenates there was an increased expression of Wnt9b in female rats compared to male. ZSF1 female rats seem to express more Wnt9b than CD rats. TGF-β increased the expression of Tenascin C in TKPTS cells while in kidney homogenates Tenascin C expression was greater in female ZSF rats than males.
We conclude that TKPTS and RMC grown in HG, both express increased TGF-β and thus initiate EMT and renal fibrosis. Increased expression of Wnt9b and Catenin levels observed both in in-vivo and in-vitro models examined here, underscore the role of WBCP in EMT in the progression of DKD.
