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学科主题基础医学
UT-B-deficient mice develop renal dysfunction and structural damage
Zhou, Lei1,3; Meng, Yan1; Lei, Tianluo2; Zhao, Dan1; Su, Jing1; Zhao, Xuejian1; Yang, Baoxue1,2
关键词Urea Transporter Renal Function Kidney Ut-b Knock-out
刊名BMC NEPHROLOGY
2012-01-30
DOI10.1186/1471-2369-13-6
13
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Urology & Nephrology
资助者National Natural Science Foundation of China ; Ministry of Education of China ; Doctoral Training Fund ; National Natural Science Foundation of China ; Ministry of Education of China ; Doctoral Training Fund
研究领域[WOS]Urology & Nephrology
关键词[WOS]URINARY CONCENTRATING ABILITY ; UREA TRANSPORT ; VASA-RECTA ; LACKING ; ERYTHROCYTES ; CELLS
英文摘要

Background: Urea transporter UT-B is the major urea transporter in erythrocytes and the descending vasa recta in the kidney. In this study, we investigated the effects of long-term UT-B deficiency on functional and structural defect in the kidney of 16-and 52-week-old UT-B-null mice.

Methods: UT-B-knockout mice were generated by targeted gene disruption and lacked UT-B protein expression in all organs. The urinary concentrating ability of mice was studied in terms of daily urine output, urine osmolality, and urine and plasma chemistries. Changes in renal morphology were evaluated by hematoxylin and eosin staining.

Results: The UT-B-null mice showed defective urine concentrating ability. The daily urine output in UT-B-null mice (2.5 +/- 0.1 ml) was 60% higher and urine osmolality (985 +/- 151 mosm) was significantly lower than that in wildtype mice (1463 +/- 227 mosm). The 52-week-old UT-B-null mice exhibited polyuria after water deprivation, although urine osmolality was increased. At 52 weeks of age, over 31% of UT-B-null mice exhibited renal medullary atrophy because of severe polyuria and hydronephrosis.

Conclusions: Long-term UT-B deficiency causes severe renal dysfunction and structural damage. These results demonstrate the important role of UT-B in countercurrent exchange and urine concentration.

语种英语
所属项目编号30370572 ; 30870921 ; 81170632 ; 985-2-094-121 ; 20100001110047
资助者National Natural Science Foundation of China ; Ministry of Education of China ; Doctoral Training Fund ; National Natural Science Foundation of China ; Ministry of Education of China ; Doctoral Training Fund
WOS记录号WOS:000304374200001
引用统计
被引频次:2[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/54642
专题基础医学院_药理学系
作者单位1.Jilin Univ, Prostate Dis Prevent & Treatment Res Ctr, Dept Pathophysiol, Norman Bethune Coll Med, Changchun 130023, Peoples R China
2.Peking Univ, Dept Pharmacol, Sch Basic Med Sci, Beijing 100871, Peoples R China
3.Changchun Univ Chinese Med, Affiliated Hosp, Dept Pathol, Changchun, Peoples R China
推荐引用方式
GB/T 7714
Zhou, Lei,Meng, Yan,Lei, Tianluo,et al. UT-B-deficient mice develop renal dysfunction and structural damage[J]. BMC NEPHROLOGY,2012,13.
APA Zhou, Lei.,Meng, Yan.,Lei, Tianluo.,Zhao, Dan.,Su, Jing.,...&Yang, Baoxue.(2012).UT-B-deficient mice develop renal dysfunction and structural damage.BMC NEPHROLOGY,13.
MLA Zhou, Lei,et al."UT-B-deficient mice develop renal dysfunction and structural damage".BMC NEPHROLOGY 13(2012).
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