Related Experiment Video For Hyperuricemia mouse model
Updated: Jul 5, 2025
Quantitative Real-Time PCR Evaluation of microRNA Expressions in Mouse Kidney with Unilateral Ureteral Obstruction
Published on: August 27, 2020
A stable liver-specific urate oxidase gene knockout hyperuricemia mouse model finds activated hepatic de novo purine
Lei Pang1, Ningning Liang2, Changgui Li1
1Institute of Metabolic Diseases, Qingdao University, Qingdao, China; Shandong Provincial Key Laboratory of Metabolic Diseases, Qingdao Key Laboratory of Gout, the Affiliated Hospital of Qingdao University, Qingdao, China.
Abstract:
Urate oxidase (Uox)-deficient mice could be an optimal animal model to study hyperuricemia and associated disorders. We develop a liver-specific conditional knockout Uox-deficient (UoxCKO) mouse using the Cre/loxP gene targeting system. These UoxCKO mice spontaneously developed hyperuricemia with accumulated serum urate metabolites. Blocking urate degradation, the UoxCKO mice showed significant de novo purine biosynthesis (DNPB) in the liver along with amidophosphoribosyltransferase (Ppat). Pegloticase and allopurinol reversed the elevated serum urate (SU) levels in UoxCKO mice and suppressed the Ppat up-regulation. Although urate nephropathy occurred in 30-week-old UoxCKO mice, 90 % of Uox-deficient mice had a normal lifespan without pronounced urate transport abnormality. Thus, UoxCKO mice are a stable model of human hyperuricemia. Activated DNPB in the UoxCKO mice provides new insights into hyperuricemia, suggesting increased SU influences purine synthesis.
