The Serum and Glucocorticoid-Regulated Kinase 1 in Hypoxic Renal Injury
| Autor: | Matthias Strobl, Christoph Schmaderer, Marcel Roos, Uwe Heemann, Bettina Wagner, Dietmar Kuhl, Almut Grenz, Florian Lang, Krishna M. Boini, Jens Lutz, Krisztina Rusai |
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| Rok vydání: | 2009 |
| Předmět: |
Male
Physiology Apoptosis Serine threonine protein kinase Protein Serine-Threonine Kinases Biology Cell Line Immediate-Early Proteins Rats Sprague-Dawley Mice In Situ Nick-End Labeling medicine Animals Humans Phosphorylation Protein kinase B Mice Knockout Kidney Renal ischemia urogenital system Kinase Akt/PKB signaling pathway Molecular biology Cell Hypoxia ddc Rats Hypoxia Ischemia/reperfusion SGK1 medicine.anatomical_structure Kidney Diseases |
| Zdroj: | Cellular Physiology and Biochemistry. 24:577-584 |
| ISSN: | 1421-9778 1015-8987 |
| DOI: | 10.1159/000257527 |
| Popis: | The serum- and glucocorticoid-inducible kinase 1 (SGK1) is a serine threonine protein kinase activated through the phosphatidylinositol 3-kinase (PI3-kinase) pathway and counteracting apoptosis. Protein expression and activation of SGK1 are increased in various models of cell stress. The present study explored the role of SGK1 in renal hypoxia/ischemia induced apoptosis. HEK 293 cells were exposed in vitro to hypoxia/reoxygenation (H/R), which increased SGK1 transcript levels, SGK1 protein abundance and SGK1 phosphorylation. H/R injury further enhanced the percentage of apoptotic cells, an effect significantly blunted by prior SGK1 overexpression. In vivo renal ischemia/reperfusion (I/R) injury increased SGK1 transcript levels and SGK1 protein abundance. I/R enhanced apoptosis, an effect significantly more pronounced in gene targeted mice lacking SGK1. In conclusion, SGK1 is up-regulated and counteracts apoptosis following H/R in vitro and ischemia in vivo. |
| Databáze: | OpenAIRE |
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