Significance and Expression of Serum and Glucocorticoid-inducible Kinase in Kidney of Mice with Diabetic Nephropathy

To investigate the expression and the role of three isoforms of Serum and Glucocorticoidinducible Kinase (SGK) in experimental diabetic nephropathy (DN), 12 male C57BL/6 mice of 8-weeks-old were divided into two groups. Streptozotocin (STZ)-induced diabetic nephropathy and normal controls were analy...

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Published inCurrent medical science Vol. 25; no. 2; pp. 170 - 173
Main Author 王全胜 张晓丽 王玉梅 邓安国 朱忠华 冯玉锡
Format Journal Article
LanguageEnglish
Published China Department of Chinese Traditional Medicine, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China%Department of Nephrology , Union Hospital, Tongji Medical College, Huazhong University of Science and Technology , Wuhan 430022, China 2005
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Summary:To investigate the expression and the role of three isoforms of Serum and Glucocorticoidinducible Kinase (SGK) in experimental diabetic nephropathy (DN), 12 male C57BL/6 mice of 8-weeks-old were divided into two groups. Streptozotocin (STZ)-induced diabetic nephropathy and normal controls were analyzed at the end of the 4th week after the induction of diabetes. Renal hemodynamics and histological studies were performed. The expression of SGK1 mRNA, SGK2 mRNA and SGK3 mRNA of kidney cortex were measured by RT-PCR, and the cortical SGK1 protein was detected with Western blotting. Our results showed that the blood glucose, blood HbA1c, 24h urinary protein, creatinine clearance and the renal index were all increased in DN group. More extracellular matrix (ECM) accumulation was observed. The level of cortical SGK1 mRNA and protein were up-regulated in DN group in comparison with control group. SGK2 and SGK3 mRNA were elevated in DN mice. In DN, mRNA level of three SGK isoforms and SGK1 protein were increased significantly. It is concluded that SGKs may contribute to the early renal injury of DN.
Bibliography:42-1679/R
R587.1
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ISSN:1672-0733
2096-5230
1993-1352
2523-899X
DOI:10.1007/BF02873568