Document Type : Original Article(s)

Authors

• Wiwit Ananda Wahyu Setyaningsih ¹
• Nur Arfian ²
• Efrayim Suryadi
• Muhammad Mansyur Romi
• Untung Tranggono
• Dwi Cahyani Ratna Sari

¹ Department of Anatomy Faculty of Medicine, Universitas Gadjah Mada, Yogyakarta, Indonesia

² Department of Anatomy Faculty of Medicine, Universitas Gadjah Mada, Yogyakarta, Pharmaco Street, North Sekip, Yogyakarta 55281, Indonesia

Abstract

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

Keywords

• Hyperuricemia
• Tubular injury
• E-cadherin gene expression
• Vimentin
• Gene expression
• Wnt5a/Ror2