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1 NIDDK, National Institute of Health, Bethesda, MD, USA; Division of Nephrology, University of Utah and Veterans Affairs Medical Center, Salt Lake City, UT, USA
2 NIDDK, National Institute of Health, Bethesda, MD, USA
3 Division of Nephrology, University of Utah and Veterans Affairs Medical Center, Salt Lake City, UT, USA
* To whom correspondence should be addressed. E-mail: Tianxin.Yang{at}hsc.utah.edu.
The present study was undertaken to determine whether the severity of renal failure or hypertension in homozygous COX-2-deficient mice (COX-2-/-) is affected by genetic background or gender. COX-2 deletion was introduced into three congenic genetic backgrounds, 129/Sv (129/COX-2-/-), C57/BL6 (C57/COX-2-/-), and BALB/c (BALB/COX-2-/-), by backcrossing the original mixed background knockout mice with the respective inbred strains for 9 or 10 generations. Evaluation of the severity of hypertension and renal failure was performed in knockout and wild type mice at the age of 2.5-3.5 months. Blood pressure measured by tail cuff plethysmography was significantly elevated in the male 129/COX-2-/- (165.8 ± 9.2 vs. 116 ± 5.1 mmHg, p<0.05), and to a much lesser extent in the female 129/COX-2-/- (127.4 ± 3.3 vs. 102.4 ± 3.3), whereas it was unchanged in the C57- or BALB/COX-2-/- mice regardless of gender. Urinary excretion of albumin, determined by EIA, was remarkably increased in the 129/Cox-2-/- (16.4 ± 4.1 vs. 0.16 ± 0.043 mg albumin/mg creatinine, p<0.001), and to a lesser extent in the male C57/COX-2-/- (0.595 ± 0.416 vs. 0.068 ± 0.019). Albumin excretion was not elevated in the male BALB/COX-2-/- or in female COX-2-/- mice on any of the three genetic backgrounds. Histological analysis showed abundant protein casts, dilated tubules, and infiltration of inflammatory cells in the male 129/COX-2-/- mice, but not in COX-2-/- mice in other strains or gender. However, the presence of small glomeruli in the nephrogenic zone was observed in all strains of COX-2 KO mice, regardless of genetic background and gender. Therefore, we conclude that the severity of hypertension and renal failure in COX-2-deficient mice is influenced by genetic background and gender, whereas the incomplete maturation of outer cortical nephrons appears to be independent of genetic background effects.
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