Up-regulation of the human serum and glucocorticoid-dependent kinase 1 in glomerulonephritis

被引:33
作者
Friedrich, B
Wärntges, S
Klingel, K
Sauter, M
Kandolf, R
Risler, T
Müller, GA
Witzgall, R
Kriz, W
Gröne, HJ
Lang, F
机构
[1] Univ Tubingen, Dept Physiol, D-72076 Tubingen, Germany
[2] Univ Tubingen, Dept Mol Pathol, D-72076 Tubingen, Germany
[3] Univ Tubingen, Dept Nephrol, D-72076 Tubingen, Germany
[4] Univ Gottingen, Dept Nephrol & Rheumatol, Gottingen, Germany
[5] Univ Heidelberg, Dept Anat, Heidelberg, Germany
[6] Deutsch Krebsforschungszentrum, D-6900 Heidelberg, Germany
关键词
glomerulonephritis; cell volume regulation; SGK1;
D O I
10.1159/000066794
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
Glomerulonephritis is paralleled by excessive formation of transforming growth factor-beta (TGF-beta), which participates in the pathophysiology of the disease. Recently, a novel downstream target of TGF-beta has been identified, i.e. the human serum and glucocorticoid-dependent kinase 1 (hSGK1), a serine/threonine kinase participating in the regulation of Na+ transport. The present study was performed to elucidate transcriptional regulation of hSGK1 in glomerulonephritis. To this end, in situ hybridization was performed in biopsies from patients with clinical diagnosis of glomerulonephritis. hSGK1 transcript levels were moderately enhanced in 5 out of 9 patients and strongly enhanced in 4 out of 9 patients. Distal nephron epithelial cell hSGK1 transcript levels were low or absent in 7 of the 9 patients but markedly enhanced in 2 of the 9 patients. In conclusion, glomerulonephritis leads to glomerular and in some cases to epithelial up-regulation of hSGK1 transcription. Copyright (C) 2002 S. Karger AG, Basel.
引用
收藏
页码:303 / 307
页数:5
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