Renal pathology resulting from PGHS-2 gene ablation in DBA/B6 mice.

Kidneys of prostaglandin H synthase-2 (PGHS-2) null mice fail to develop normally, leading to renal insufficiency. We have found that in a mixed DBA/B6 background, the lack of a functional PGHS-2 gene causes less severe renal pathology than was reported previously for PGHS-2 null mice in a B6 genetic background. The increase in blood urea nitrogen in the DBA/B6 strain of PGHS-2 null mice was significantly lower than reported for B6 PGHS-2 null mice (200% versus 270%). Cystic changes in DBA/B6 PGHS-2 null mice were also less severe. The DBA/B6 PGHS-2 null adult mice did not die from renal failure, unlike their B6/PGHS-2 counterparts that showed excessive neonatal and adult deaths. Therefore, DBA/B6 PGHS-2 null may be highly suitable to study the functional consequences of the lack of PGHS-2 in the kidney due to their less severe pathology and greater survival.