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The serum and glucocorticoid-regulated kinase 1 in hypoxic renal injury

  • Krisztina Rusai
  • , Bettina Wagner
  • , Marcel Roos
  • , Christoph Schmaderer
  • , Matthias Strobl
  • , Krishna M. Boini
  • , Almut Grenz
  • , Dietmar Kuhl
  • , Uwe Heemann
  • , Florian Lang
  • , Jens Lutz
  • Semmelweis University
  • Technical University of Munich
  • University of Tübingen
  • University of Colorado Denver
  • Free University of Berlin

Research output: Contribution to journalArticlepeer-review

24 Scopus citations

Abstract

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.

Original languageEnglish
Pages (from-to)577-584
Number of pages8
JournalCellular Physiology and Biochemistry
Volume24
Issue number5-6
DOIs
StatePublished - 2009

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

  1. SDG 3 - Good Health and Well-being
    SDG 3 Good Health and Well-being

Keywords

  • Apoptosis
  • Hypoxia
  • Ischemia/reperfusion
  • Kidney
  • SGK1

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