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Hyperuricemia Induces Wnt5a/Ror2 Gene Expression, Epithelial–Mesenchymal Transition, and Kidney Tubular Injury in Mice | ||
Iranian Journal of Medical Sciences | ||
مقاله 6، دوره 43، شماره 2، خرداد 2018، صفحه 164-173 اصل مقاله (1.39 M) | ||
نوع مقاله: Original Article(s) | ||
شناسه دیجیتال (DOI): 10.30476/ijms.2018.40525 | ||
نویسندگان | ||
Wiwit Ananda Wahyu Setyaningsih1؛ Nur Arfian* 2؛ Efrayim Suryadi؛ Muhammad Mansyur Romi؛ Untung Tranggono؛ Dwi Cahyani Ratna Sari | ||
1Department of Anatomy Faculty of Medicine, Universitas Gadjah Mada, Yogyakarta, Indonesia | ||
2Department of Anatomy Faculty of Medicine, Universitas Gadjah Mada, Yogyakarta, Pharmaco Street, North Sekip, Yogyakarta 55281, Indonesia | ||
چکیده | ||
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 | ||
کلیدواژهها | ||
Hyperuricemia؛ Tubular injury؛ E-cadherin gene expression؛ Vimentin؛ Gene expression؛ Wnt5a/Ror2 | ||
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