The serum and glucocorticoid-regulated kinase 1 in hypoxic renal injury.
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The serum and glucocorticoid-regulated kinase 1 in hypoxic renal injury. / Rusai, Krisztina; Wagner, Bettina; Roos, Marcel; Schmaderer, Christoph; Strobl, Matthias; Boini, Krishna M; Grenz, Almut; Kuhl, Dietmar; Heemann, Uwe; Lang, Florian; Lutz, Jens.
In: CELL PHYSIOL BIOCHEM, Vol. 24, No. 5-6, 5-6, 2009, p. 577-584.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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T1 - The serum and glucocorticoid-regulated kinase 1 in hypoxic renal injury.
AU - Rusai, Krisztina
AU - Wagner, Bettina
AU - Roos, Marcel
AU - Schmaderer, Christoph
AU - Strobl, Matthias
AU - Boini, Krishna M
AU - Grenz, Almut
AU - Kuhl, Dietmar
AU - Heemann, Uwe
AU - Lang, Florian
AU - Lutz, Jens
PY - 2009
Y1 - 2009
N2 - 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.
AB - 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.
U2 - 10.1159/000257527
DO - 10.1159/000257527
M3 - SCORING: Zeitschriftenaufsatz
VL - 24
SP - 577
EP - 584
JO - CELL PHYSIOL BIOCHEM
JF - CELL PHYSIOL BIOCHEM
SN - 1015-8987
IS - 5-6
M1 - 5-6
ER -