Uox-KO (Prolonged) Mice

The Uox gene is located on mouse chromosome 3, and exon 3~4 was deleted.

The Uox-KO (Prolonged) mice can be used in research on hyperuricemia, gout and related diseases, and other metabolic and renal diseases.

It has been reported that homozygous Uox KO mice die within a few weeks of birth and need to be maintained with drugs such as allopurinol after birth ^[2].

1. The growth curve

Figure 1. Detection of body weight in Uox KO mice and wild-type mice. The body weight of mice was measured weekly after grouping. The results showed that there was no significant difference in body weight between Uox KO mice and wild-type control (Control) mice, and allopurinol treatment had no significant effect on the body weight of Uox KO mice.

2. The survival curve

Figure 2. Survival curves of Uox KO mice compared with wild-type mice. The survival status of mice was checked weekly after grouping. The results showed that the survival rate of Uox KO mice remained unchanged after decreasing to 75% at week 5 compared to wild-type control (Control) mice, while the survival rate of allopurinol-treated Uox KO mice decreased only at week 18 and decreased to 66.67% at week 22. This result suggests that the administration of allopurinol to Uox KO mice improves survival by 18 weeks.

3. The Uox expression

Figure 3. Detection of Uox mRNA expression in Uox KO mice and wild-type mice (WT). RT-PCR was utilized to detect the expression of Uox in Uox KO mice and wild-type mice (WT), respectively, and the results showed that there was no expression of Uox in Uox KO mice.

4. Blood biochemical indexes

Figure 4. Blood biochemical analysis of Uox KO mice and wild-type mice. The results showed that the Blood Urea Nitrogen (BUN), Creatinine (CREA), and Uric Acid (UA) levels in Uox KO mice were elevated to different degrees compared with wild-type control mice, showing the characteristics of hyperuricemia. In contrast, allopurinol-treated Uox KO mice had decreased levels of urea nitrogen, creatinine, and, uric acid compared with untreated Uox KO mice.
Note: Allopurinol treatments are for breeding needs only and not for efficacy studies.

5. Renal pathology

Figure 5. Morphological changes in the appearance of kidneys of Uox KO mice and wild-type mice. Compared to wild-type control (Control) mice, Uox KO mice had renal lesions with significant hydronephrosis, and allopurinol-treated Uox KO mice also had the hydronephrosis phenotype.

6. H&E staining of the kidney

Figure 6. Kidney H&E staining of Uox KO mice and wild-type mice. Compared to wild-type control (Control) mice, Uox KO mice had lesions in the kidney with blue lesions in the outer cortex, and the same lesion phenotype was present in allopurinol-treated Uox KO mice.

7. Summary

Uox-KO (Prolonged) mice, a model of hyperuricemia disease, were constructed by knocking out the Uox gene. Phenotypic test results showed that compared with wild-type mice, the survival rate of Uox KO mice was decreased, and the contents of urea nitrogen, creatinine, and uric acid were increased to varying degrees. Adding 100mg/L allopurinol to the drinking water throughout pregnancy and fostering period of Uox KO mice can significantly increase their survival rate. This model can be used for subsequent studies of hyperuricemia, providing a powerful and effective tool for metabolic disease research.