2004Zhonghua shenzangbing zazhiRequires access

Expression of serum and glucocorticoid-inducible kinase and its potential role in murine diabetic nephropathy

Feng Yu-x

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Abstract

Objective To investigate the expression and potential role of serum and glucocorticoid inducible kinase (SGK) in diabetic nephropathy(DN) . Methods Twelve C57BL/6 mice were divided into two groups: DN group, induced by streptozotocin(STZ) 150 mg/kg peritoneal injection and normal control group (NG), treated with saline peritoneal injection. The mice were sacrificed at the end of the 4th week. The metabolic data were measured at week 4. Cortical SGK1 protein was detected by Western blotting. The mRNA expression of cortical SGK1, SGK2, SGK3, collagen(Col) Iα2, fibronectin(FN) and TGF-β1 was examined by RT-PCR. Renal function was evaluated by calculating Ccr. Serum and urinary creatinine were measured by autoanalyzer Hitachi 7150. Glomerular pathological changes were detected with periodic acid-schiff staining. Results As compared to NG, 24 h urinary protein, Ccr and the ratio of kidney weight were all increased in DN group. More extracellular matrix (ECM) accumulation was observed. Col I α2, FN and TGF-β1 mRNA were also up-regulated in DN mice. The levels of cortex SGK1mRNA and protein as well as SGK2 and SGK3 mRNA were up-regulated in DN group. The mRNA of SGK1, SGK2 and SGK3 was positively correlated with the mRNA of Col Iα2, FN and TGF-β1. Conclusions In DN renal cortex, the high expression of SGK is accompanied with ECM accumulation, and positively correlated with the Col Iα2, FN and TGF-β1 mRNA. The high levels of SGK in renal cortex may contribute to early renal injury of DN.

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Objective To investigate the expression and potential role of serum and glucocorticoid inducible kinase (SGK) in diabetic nephropathy(DN) . Methods Twelve C57BL/6 mice were divided into two groups: DN group, induced by streptozotocin(STZ) 150 mg/kg peritoneal injection and normal control group (NG), treated with saline peritoneal injection. The mice were sacrificed at the end of the 4th week. The metabolic data were measured at week 4. Cortical SGK1 protein was detected by Western blotting. The mRNA expression of cortical SGK1, SGK2, SGK3, collagen(Col) Iα2, fibronectin(FN) and TGF-β1 was examined by RT-PCR. Renal function was evaluated by calculating Ccr. Serum and urinary creatinine were measured by autoanalyzer Hitachi 7150. Glomerular pathological changes were detected with periodic acid-schiff staining. Results As compared to NG, 24 h urinary protein, Ccr and the ratio of kidney weight were all increased in DN group. More extracellular matrix (ECM) accumulation was observed. Col I α2, FN and TGF-β1 mRNA were also up-regulated in DN mice. The levels of cortex SGK1mRNA and protein as well as SGK2 and SGK3 mRNA were up-regulated in DN group. The mRNA of SGK1, SGK2 and SGK3 was positively correlated with the mRNA of Col Iα2, FN and TGF-β1. Conclusions In DN renal cortex, the high expression of SGK is accompanied with ECM accumulation, and positively correlated with the Col Iα2, FN and TGF-β1 mRNA. The high levels of SGK in renal cortex may contribute to early renal injury of DN.

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Available abstract

Objective To investigate the expression and potential role of serum and glucocorticoid inducible kinase (SGK) in diabetic nephropathy(DN) . Methods Twelve C57BL/6 mice were divided into two groups: DN group, induced by streptozotocin(STZ) 150 mg/kg peritoneal injection and normal control group (NG), treated with saline peritoneal injection. The mice were sacrificed at the end of the 4th week. The metabolic data were measured at week 4. Cortical SGK1 protein was detected by Western blotting. The mRNA expression of cortical SGK1, SGK2, SGK3, collagen(Col) Iα2, fibronectin(FN) and TGF-β1 was examined by RT-PCR. Renal function was evaluated by calculating Ccr. Serum and urinary creatinine were measured by autoanalyzer Hitachi 7150. Glomerular pathological changes were detected with periodic acid-schiff staining. Results As compared to NG, 24 h urinary protein, Ccr and the ratio of kidney weight were all increased in DN group. More extracellular matrix (ECM) accumulation was observed. Col I α2, FN and TGF-β1 mRNA were also up-regulated in DN mice. The levels of cortex SGK1mRNA and protein as well as SGK2 and SGK3 mRNA were up-regulated in DN group. The mRNA of SGK1, SGK2 and SGK3 was positively correlated with the mRNA of Col Iα2, FN and TGF-β1. Conclusions In DN renal cortex, the high expression of SGK is accompanied with ECM accumulation, and positively correlated with the Col Iα2, FN and TGF-β1 mRNA. The high levels of SGK in renal cortex may contribute to early renal injury of DN.

Key concepts: Endocrinology, Internal medicine, Renal cortex, Diabetic nephropathy, SGK1, Streptozotocin, Kinase, Kidney

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