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Uox KO Mice
Product Number：C001232
Strain Name: C57BL/6JCya-Uoxem2/Cya
Genetic Background：C57BL/6JCya
Reproduction：Heterozygote x Heterozygote
Strain Description
Uricase, which is encoded by the urate oxidase (UOX) gene, has an important role in the purine metabolic pathway, and most mammals contain UOX, which breaks down uric acid, a metabolite of purine nucleotides, into allantoin, which is more soluble than uric acid. Unlike other mammals, humans lack UOX, and purine catabolism can only produce uric acid, which is subsequently excreted by the kidneys, resulting in higher serum uric acid concentrations in humans than in other mammals. When the rate of uric acid production exceeds the excretory capacity of the kidneys, the serum uric acid level increases significantly, resulting in hyperuricemia.UOX can significantly reduce plasma uric acid levels and can treat gout and kidney disease secondary to hyperuricemia, among others[1].
This strain is a Uox gene deletion mouse, in which the synthesis of uricase is blocked in the mouse organism and the hyperuricemia phenotype occurs spontaneously. The heterozygous Uox KO mice are viable and fertile. This model was constructed by knocking out Exon 2~4 of the Uox gene. A similar strain is Uox-KO (Prolonged) (Catalog number: C001393. Exon 3~4 was deleted). Uox-KO (Prolonged) mice have milder symptoms of hyperuricemia after allopurinol treatment, longer lifespan, and higher survival rate in homozygotes. In contrast, the disease phenotype of Uox KO mice is more severe and the disease progresses faster.
The Uox gene is located on mouse chromosome 3, and Exon 2~4 of this gene was deleted.
The Uox KO mice can be used in the study of hyperuricemia, gout, and its related kidney disease.
Approximately 65% of homozygous Uox KO mice die successively after a few weeks of life and therefore need to be maintained after birth with drugs such as allopurinol[2].
1. The Growth Curve
Figure 1. Growth curve of homozygous Uox KO mice (Uox-/-). Mice were grouped and given different concentrations of allopurinol, and their body weight was measured weekly. The trend in body weight change was similar in all groups from 3 to 8 weeks, with no significant difference. At 9-10 weeks, the body weight of mice in the G3 group decreased and then remained unchanged.
(G1: Uox-/- mice + normal drinking, G2: Uox-/- mice + low dose allopurinol drinking, G3: Uox-/- mice + medium dose allopurinol drinking, G4: Uox-/- mice + high dose allopurinol drinking, G5: WT mice + normal drinking, Same below)
2. The survival curve
Figure 2. Survival curve of homozygous Uox KO mice. Mice were divided into groups and given different concentrations of allopurinol, and their survival status was monitored weekly. The results showed that the survival rate of the G2 low-dose allopurinol group remained at 100%, while the survival rates of the other three groups began to decline after 4 weeks. At 10 weeks, the survival rates of the G1, G3, and G4 groups were 75%, 25%, and 25%, respectively.
Internal testing data showed that the blood biochemical levels of urea nitrogen (BUN), creatinine (CREA), and uric acid (UA) in this strain of mice were elevated to varying degrees compared to wild-type mice. The mice were given drinking water with a concentration of 100 mg/L of allopurinol throughout the pregnancy and foster period, and the medication was stopped after the pups were weaned. This treatment could minimally reduce some blood biochemical indicators of the Uox KO mice and prolong their survival, but the improvement effect of allopurinol on blood biochemical indicators and survival status in this strain is not as good as that in Uox-KO (Prolonged) mice (Catalog Number: C001393). Therefore, if the research needs to observe and experiment on mice for a long time, it is recommended to choose Uox-KO (Prolonged) mice and administer allopurinol according to actual conditions.
References
[1] Lu J , Dalbeth N, Yin H , et al. Mouse models for human hyperuricaemia: a critical review[J]. Nature Reviews Rheumatology, 2019, 15(Suppl. 10):1.
[2] Wu X . Hyperuricemia and urate nephropathy in urate oxidase-deficient mice[J]. Proc Natl Acad Sci U S A, 1994, 91.
