TY - JOUR ID - 40525 TI - Hyperuricemia Induces Wnt5a/Ror2 Gene Expression, Epithelial–Mesenchymal Transition, and Kidney Tubular Injury in Mice JO - Iranian Journal of Medical Sciences JA - IJMS LA - en SN - 0253-0716 AU - Setyaningsih, Wiwit Ananda Wahyu AU - Arfian, Nur AU - Suryadi, Efrayim AU - Romi, Muhammad Mansyur AU - Tranggono, Untung AU - Sari, Dwi Cahyani Ratna AD - Department of Anatomy Faculty of Medicine, Universitas Gadjah Mada, Yogyakarta, Indonesia AD - Department of Anatomy Faculty of Medicine, Universitas Gadjah Mada, Yogyakarta, Pharmaco Street, North Sekip, Yogyakarta 55281, Indonesia AD - Y1 - 2018 PY - 2018 VL - 43 IS - 2 SP - 164 EP - 173 KW - Hyperuricemia KW - Tubular injury KW - E-cadherin gene expression KW - Vimentin KW - Gene expression KW - Wnt5a/Ror2 DO - 10.30476/ijms.2018.40525 N2 - Background: Hyperuricemia contributes to kidney injury, characterized by tubular injury with epithelial–mesenchymal transition (EMT). Wnt5a/Ror2 signaling drives EMT in many kidney pathologies. This study sought to evaluate the involvement of Wnt5a/Ror2 in hyperuricemia-induced EMT in kidney tubular injury.Methods: A hyperuricemia model was performed in male Swiss background mice (3 months old, 30–40 g) with daily intraperitoneal injections of 125 mg/kg body weight (BW) of uric acid. The mice were terminated on day 7 (UA7, n=5) and on day 14 (UA14, n=5). Allopurinol groups (UAl7 and UAl14, each n=5) were added with oral 50 mg/kg BW of allopurinol treatment. The serum uric acid level was quantified, and tubular injury was assessed based on PAS staining. Reverse transcriptase-PCR was done to quantify Wnt5a, Ror2, E-cadherin, and vimentin expressions. IHC staining was done for E-cadherin and collagen I. We used the Shapiro–Wilk for normality testing and one-way ANOVA for variance analysis with a P UR - https://ijms.sums.ac.ir/article_40525.html L1 - https://ijms.sums.ac.ir/article_40525_6d96ac3f398b941dd16064315fdef106.pdf ER -