Expression of the serine/threonine kinase hSGK1 in chronic viral hepatitis

Sophie Fillon; Karin Klingel; Simone Wärntges; Martina Sauter; Sabine Gabrysch; Sabine Pestel; Valerie Tanneur; Siegfried Waldegger; Anette Zipfel; Richard Viebahn; Dieter Häussinger; Stefan Bröer; Reinhard Kandolf; Florian Lang

doi:10.1159/000047826

Expression of the serine/threonine kinase hSGK1 in chronic viral hepatitis

Sophie Fillon, Karin Klingel, Simone Wärntges, Martina Sauter, Sabine Gabrysch, Sabine Pestel, Valerie Tanneur, Siegfried Waldegger, Anette Zipfel, Richard Viebahn, Dieter Häussinger, Stefan Bröer, Reinhard Kandolf, Florian Lang^*

^*Corresponding author for this work

Research output: Contribution to journal › Article › peer-review

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Abstract

The human serine/threonine kinase hSGK1 is expressed ubiquitously with highest transcript levels in pancreas and liver. This study has been performed to determine the hSGK1 distribution in normal liver and its putative role in fibrosing liver disease. HSGK1-localization was determined by in situ hybridization, regulation of hSGK1-transcription by Northern blotting, fibronectin synthesis and hSGK1 phosphorylation by Western blotting. In normal liver hSGK1 was mainly transcribed by Kupffer cells. In liver tissue from patients with chronic viral hepatitis, hSGK1 transcript levels were excessively high in numerous activated Kupffer cells and inflammatory cells localized within fibrous septum formations. HSGK1 transcripts were also detected in activated hepatic stellate cells. Accordingly, Western blotting revealed that tissue from fibrotic liver expresses excessive hSGK1 protein as compared to normal liver. TGF-β1 (2 ng/ml) increases hSGK1 transcription in both human U937 macrophages and HepG2 hepatoma cells. H ₂ O ₂ (0.3 mM) activated hSGK1 and increased fibronectin formation in HepG2 cells overexpressing hSGK1 but not in HepG2 cells expressing the inactive mutant hSGK1 ^K127R . In conclusion hSGK1 is upregulated by TGF-β1 during hepatitis and may contribute to enhanced matrix formation during fibrosing liver disease.

Original language	English
Pages (from-to)	47-54
Number of pages	8
Journal	Cellular Physiology and Biochemistry
Volume	12
Issue number	1
DOIs	https://doi.org/10.1159/000047826
Publication status	Published - 2002

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title = "Expression of the serine/threonine kinase hSGK1 in chronic viral hepatitis",

abstract = " The human serine/threonine kinase hSGK1 is expressed ubiquitously with highest transcript levels in pancreas and liver. This study has been performed to determine the hSGK1 distribution in normal liver and its putative role in fibrosing liver disease. HSGK1-localization was determined by in situ hybridization, regulation of hSGK1-transcription by Northern blotting, fibronectin synthesis and hSGK1 phosphorylation by Western blotting. In normal liver hSGK1 was mainly transcribed by Kupffer cells. In liver tissue from patients with chronic viral hepatitis, hSGK1 transcript levels were excessively high in numerous activated Kupffer cells and inflammatory cells localized within fibrous septum formations. HSGK1 transcripts were also detected in activated hepatic stellate cells. Accordingly, Western blotting revealed that tissue from fibrotic liver expresses excessive hSGK1 protein as compared to normal liver. TGF-β1 (2 ng/ml) increases hSGK1 transcription in both human U937 macrophages and HepG2 hepatoma cells. H 2 O 2 (0.3 mM) activated hSGK1 and increased fibronectin formation in HepG2 cells overexpressing hSGK1 but not in HepG2 cells expressing the inactive mutant hSGK1 K127R . In conclusion hSGK1 is upregulated by TGF-β1 during hepatitis and may contribute to enhanced matrix formation during fibrosing liver disease.",

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author = "Sophie Fillon and Karin Klingel and Simone W{\"a}rntges and Martina Sauter and Sabine Gabrysch and Sabine Pestel and Valerie Tanneur and Siegfried Waldegger and Anette Zipfel and Richard Viebahn and Dieter H{\"a}ussinger and Stefan Br{\"o}er and Reinhard Kandolf and Florian Lang",

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AU - Fillon, Sophie

AU - Klingel, Karin

AU - Wärntges, Simone

AU - Sauter, Martina

AU - Gabrysch, Sabine

AU - Pestel, Sabine

AU - Tanneur, Valerie

AU - Waldegger, Siegfried

AU - Zipfel, Anette

AU - Viebahn, Richard

AU - Häussinger, Dieter

AU - Bröer, Stefan

AU - Kandolf, Reinhard

AU - Lang, Florian

PY - 2002

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N2 - The human serine/threonine kinase hSGK1 is expressed ubiquitously with highest transcript levels in pancreas and liver. This study has been performed to determine the hSGK1 distribution in normal liver and its putative role in fibrosing liver disease. HSGK1-localization was determined by in situ hybridization, regulation of hSGK1-transcription by Northern blotting, fibronectin synthesis and hSGK1 phosphorylation by Western blotting. In normal liver hSGK1 was mainly transcribed by Kupffer cells. In liver tissue from patients with chronic viral hepatitis, hSGK1 transcript levels were excessively high in numerous activated Kupffer cells and inflammatory cells localized within fibrous septum formations. HSGK1 transcripts were also detected in activated hepatic stellate cells. Accordingly, Western blotting revealed that tissue from fibrotic liver expresses excessive hSGK1 protein as compared to normal liver. TGF-β1 (2 ng/ml) increases hSGK1 transcription in both human U937 macrophages and HepG2 hepatoma cells. H 2 O 2 (0.3 mM) activated hSGK1 and increased fibronectin formation in HepG2 cells overexpressing hSGK1 but not in HepG2 cells expressing the inactive mutant hSGK1 K127R . In conclusion hSGK1 is upregulated by TGF-β1 during hepatitis and may contribute to enhanced matrix formation during fibrosing liver disease.

AB - The human serine/threonine kinase hSGK1 is expressed ubiquitously with highest transcript levels in pancreas and liver. This study has been performed to determine the hSGK1 distribution in normal liver and its putative role in fibrosing liver disease. HSGK1-localization was determined by in situ hybridization, regulation of hSGK1-transcription by Northern blotting, fibronectin synthesis and hSGK1 phosphorylation by Western blotting. In normal liver hSGK1 was mainly transcribed by Kupffer cells. In liver tissue from patients with chronic viral hepatitis, hSGK1 transcript levels were excessively high in numerous activated Kupffer cells and inflammatory cells localized within fibrous septum formations. HSGK1 transcripts were also detected in activated hepatic stellate cells. Accordingly, Western blotting revealed that tissue from fibrotic liver expresses excessive hSGK1 protein as compared to normal liver. TGF-β1 (2 ng/ml) increases hSGK1 transcription in both human U937 macrophages and HepG2 hepatoma cells. H 2 O 2 (0.3 mM) activated hSGK1 and increased fibronectin formation in HepG2 cells overexpressing hSGK1 but not in HepG2 cells expressing the inactive mutant hSGK1 K127R . In conclusion hSGK1 is upregulated by TGF-β1 during hepatitis and may contribute to enhanced matrix formation during fibrosing liver disease.

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KW - Fibronectin

KW - HepG2 cells

KW - Liver fibrosis

KW - Macrophages

KW - TGF-β1

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JO - Cellular Physiology and Biochemistry

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ER -

Expression of the serine/threonine kinase hSGK1 in chronic viral hepatitis

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