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.
Laulederkind
Stanley J F
SJ
Department of Veterans Affairs Medical Center, The University of Tennessee, Memphis 38104, USA.
Wall
Barry M
BM
Ballou
Leslie R
LR
Raghow
Rajendra
R
D000818:Animals; D001806:Blood Urea Nitrogen; D003404:Creatinine / Q000097:blood; D051546:Cyclooxygenase 2; D006400:Hematocrit; D007527:Isoenzymes / Q000172:deficiency* / Q000235:genetics; D007668:Kidney / Q000002:abnormalities* / Q000473:pathology / Q000503:physiopathology; D051379:Mice; D008811:Mice, Inbred DBA; D018345:Mice, Knockout; D009929:Organ Size; D011451:Prostaglandin-Endoperoxide Synthases / Q000172:deficiency* / Q000235:genetics
D007527:Isoenzymes; D003404:Creatinine; D051546:Cyclooxygenase 2; D011451:Prostaglandin-Endoperoxide Synthases