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

被引：6

作者：

Laulederkind, SJF

Wall, BM

Ballou, LR

Raghow, R

机构：

[1] Univ Tennessee, Dept Vet Affairs Med Ctr, Res Serv 151, Memphis, TN 38104 USA

[2] Univ Tennessee, Ctr Hlth Sci, Dept Med, Memphis, TN 38163 USA

[3] Univ Tennessee, Ctr Hlth Sci, Dept Mol Sci, Memphis, TN 38163 USA

[4] Univ Tennessee, Ctr Hlth Sci, Dept Pharmacol, Memphis, TN 38163 USA

来源：

PROSTAGLANDINS & OTHER LIPID MEDIATORS | 2002年 / 70卷 / 1-2期

关键词：

prostaglandin H synthase-2; murine; kidney; hypoplasia;

D O I：

10.1016/S0090-6980(02)00063-1

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

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/136 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. (C) 2002 Elsevier Science Inc. All rights reserved.

引用

页码：161 / 168

页数：8

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