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4. Growth-hormone–induced signal transducer and activator of transcription 5 signaling causes gigantism, inflammation, and premature death but protects mice from aggressive liver cancer

Author

Friedbichler, Katrin, Themanns, Madeleine, Mueller, Kristina M., Schlederer, Michaela, Kornfeld, Jan-Wilhelm, Terracciano, Luigi M., Kozlov, Andrey V., Haindl, Susanne, Kenner, Lukas, Kolbe, Thomas, Mueller, Mathias, Snibson, Kenneth J., Heim, Markus H., and Moriggl, Richard

Published
2012
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5. Impairment of hepatic growth hormone and glucocorticoid receptor signaling causes steatosis and hepatocellular carcinoma in mice

Author

Mueller, Kristina M., Kornfeld, Jan-Wilhelm, Friedbichler, Katrin, Blaas, Leander, Egger, Gerda, Esterbauer, Harald, Hasselblatt, Peter, Schlederer, Michaela, Haindl, Susanne, Wagner, Kay-Uwe, Engblom, David, Haemmerle, Guenter, Kratky, Dagmar, Sexl, Veronika, Kenner, Lukas, Kozlov, Andrey V., Terracciano, Luigi, Zechner, Rudolf, Schuetz, Guenther, Casanova, Emilio, Pospisilik, Andrew J., Heim, Markus H., and Moriggl, Richard

Published
2011
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7. Hepatic growth hormone - JAK2 - STAT5 signalling: Metabolic function, non-alcoholic fatty liver disease and hepatocellular carcinoma progression

Author

Kaltenecker, Doris, primary, Themanns, Madeleine, additional, Mueller, Kristina M., additional, Spirk, Katrin, additional, Suske, Tobias, additional, Merkel, Olaf, additional, Kenner, Lukas, additional, Luís, Andreia, additional, Kozlov, Andrey, additional, Haybaeck, Johannes, additional, Müller, Mathias, additional, Han, Xiaonan, additional, and Moriggl, Richard, additional

Published
2019
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8. Erratum. Adipocyte Glucocorticoid Receptor Deficiency Attenuates Aging- and HFD-Induced Obesity and Impairs the Feeding-Fasting Transition. Diabetes 2017;66:272–286

Author

Mueller, Kristina M., primary, Hartmann, Kerstin, additional, Kaltenecker, Doris, additional, Vettorazzi, Sabine, additional, Bauer, Mandy, additional, Mauser, Lea, additional, Amann, Sabine, additional, Jall, Sigrid, additional, Fischer, Katrin, additional, Esterbauer, Harald, additional, Müller, Timo D., additional, Tschöp, Matthias H., additional, Magnes, Christoph, additional, Haybaeck, Johannes, additional, Scherer, Thomas, additional, Bordag, Natalie, additional, Tuckermann, Jan P., additional, and Moriggl, Richard, additional

Published
2017
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9. Hepatic growth hormone and glucocorticoid receptor signaling in body growth, steatosis and metabolic liver cancer development

Author

Mueller, Kristina M., Themanns, Madeleine, Friedbichler, Katrin, Kornfeld, Jan-Wilhelm, Esterbauer, Harald, Tuckermann, Jan P., and Moriggl, Richard

Subjects
Glucose metabolism, Liver Neoplasms, food and beverages, Review, Biochemistry, Fatty Liver, Receptors, Glucocorticoid, Endocrinology, Growth Hormone, Animals, Humans, Growth and Development, Glucocorticoids, Molecular Biology, STAT5, Non-alcoholic fatty liver disease, Signal Transduction
Abstract

Highlights ► Conditional mouse models illuminated the role of hepatic GH-STAT5 and GC-GR signaling in liver function. ► We provide an overview of overlapping and distinct functions of hepatic GH-STAT5 and GC-GR signaling in growth/metabolism. ► Impaired hepatic GH-STAT5 signaling sensitizes hepatocytes to injury and tumorigenic transformation. ► Loss of hepatic GR function causes chronic stress, thereby aggravating liver cancer formation upon impaired STAT5 function., Growth hormone (GH) and glucocorticoids (GCs) are involved in the control of processes that are essential for the maintenance of vital body functions including energy supply and growth control. GH and GCs have been well characterized to regulate systemic energy homeostasis, particular during certain conditions of physical stress. However, dysfunctional signaling in both pathways is linked to various metabolic disorders associated with aberrant carbohydrate and lipid metabolism. In liver, GH-dependent activation of the transcription factor signal transducer and activator of transcription (STAT) 5 controls a variety of physiologic functions within hepatocytes. Similarly, GCs, through activation of the glucocorticoid receptor (GR), influence many important liver functions such as gluconeogenesis. Studies in hepatic Stat5 or GR knockout mice have revealed that they similarly control liver function on their target gene level and indeed, the GR functions often as a cofactor of STAT5 for GH-induced genes. Gene sets, which require physical STAT5–GR interaction, include those controlling body growth and maturation. More recently, it has become evident that impairment of GH-STAT5 signaling in different experimental models correlates with metabolic liver disease, ranging from hepatic steatosis to hepatocellular carcinoma (HCC). While GH-activated STAT5 has a protective role in chronic liver disease, experimental disruption of GC-GR signaling rather seems to ameliorate metabolic disorders under metabolic challenge. In this review, we focus on the current knowledge about hepatic GH-STAT5 and GC-GR signaling in body growth, metabolism, and protection from fatty liver disease and HCC development.

Published
2012
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11. Nature Communications / Disruption of STAT3 signalling promotes KRAS-induced lung tumorigenesis

Author

Grabner, Beatrice, Schramek, Daniel, Mueller, Kristina M., Moll, Herwig P., Svinka, Jasmin, Hoffmann, Thomas, Bauer, Eva, Blaas, Leander, Hruschka, Natascha, Zboray, Katalin, Stiedl, Patricia, Nivarthi, Harini, Bogner, Edith, Gruber, Wolfgang, Mohr, Thomas, Zwick, Ralf Harun, Kenner, Lukas, Poli, Valeria, Aberger, Fritz, Stoiber, Dagmar, Egger, Gerda, Esterbauer, Harald, Zuber, Johannes, Zuber, Richard, and Moriggl, Richard

Subjects
Cancer therapy, Lung cancer, Cell signalling
Abstract

STAT3 is considered to play an oncogenic role in several malignancies including lung cancer; consequently, targeting STAT3 is currently proposed as therapeutic intervention. Here we demonstrate that STAT3 plays an unexpected tumour-suppressive role in KRAS mutant lung adenocarcinoma (AC). Indeed, lung tissue-specific inactivation of Stat3 in mice results in increased KrasG12D-driven AC initiation and malignant progression leading to markedly reduced survival. Knockdown of STAT3 in xenografted human AC cells increases tumour growth. Clinically, low STAT3 expression levels correlate with poor survival and advanced malignancy in human lung AC patients with smoking history, which are prone to KRAS mutations. Consistently, KRAS mutant lung tumours exhibit reduced STAT3 levels. Mechanistically, we demonstrate that STAT3 controls NF-B-induced IL-8 expression by sequestering NF-B within the cytoplasm, thereby inhibiting IL-8-mediated myeloid tumour infiltration and tumour vascularization and hence tumour progression. These results elucidate a novel STAT3NF-BIL-8 axis in KRAS mutant AC with therapeutic and prognostic relevance. P 25599 (VLID)1838914

Published
2015

12. Hepatic Deletion of Janus Kinase 2 Counteracts Oxidative Stress in Mice

Author

Themanns, Madeleine, primary, Mueller, Kristina M., additional, Kessler, Sonja M., additional, Golob-Schwarzl, Nicole, additional, Mohr, Thomas, additional, Kaltenecker, Doris, additional, Bourgeais, Jerome, additional, Paier-Pourani, Jamile, additional, Friedbichler, Katrin, additional, Schneller, Doris, additional, Schlederer, Michaela, additional, Zebedin-Brandl, Eva, additional, Terracciano, Luigi M., additional, Han, Xiaonan, additional, Kenner, Lukas, additional, Wagner, Kay-Uwe, additional, Mikulits, Wolfgang, additional, Kozlov, Andrey V., additional, Heim, Markus H., additional, Gouilleux, Fabrice, additional, Haybaeck, Johannes, additional, and Moriggl, Richard, additional

Published
2016
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13. Adipocyte Glucocorticoid Receptor Deficiency Attenuates Aging- and HFD-Induced Obesity and Impairs the Feeding-Fasting Transition

Author

Mueller, Kristina M., primary, Hartmann, Kerstin, additional, Kaltenecker, Doris, additional, Vettorazzi, Sabine, additional, Bauer, Mandy, additional, Mauser, Lea, additional, Amann, Sabine, additional, Jall, Sigrid, additional, Fischer, Katrin, additional, Esterbauer, Harald, additional, Müller, Timo D., additional, Tschöp, Matthias H., additional, Magnes, Christoph, additional, Haybaeck, Johannes, additional, Scherer, Thomas, additional, Bordag, Natalie, additional, Tuckermann, Jan P., additional, and Moriggl, Richard, additional

Published
2016
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14. YK-4-279 effectively antagonizes EWS-FLI1 induced leukemia in a transgenic mouse model

Author

Minas, Tsion Zewdu, primary, Han, Jenny, additional, Javaheri, Tahereh, additional, Hong, Sung-Hyeok, additional, Schlederer, Michaela, additional, Saygideğer-Kont, Yasemin, additional, Çelik, Haydar, additional, Mueller, Kristina M., additional, Temel, Idil, additional, Özdemirli, Metin, additional, Kovar, Heinrich, additional, Erkizan, Hayriye Verda, additional, Toretsky, Jeffrey, additional, Kenner, Lukas, additional, Moriggl, Richard, additional, and Üren, Aykut, additional

Published
2015
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16. Disruption of STAT3 signalling promotes KRAS-induced lung tumorigenesis

Author

Grabner, Beatrice, primary, Schramek, Daniel, additional, Mueller, Kristina M., additional, Moll, Herwig P., additional, Svinka, Jasmin, additional, Hoffmann, Thomas, additional, Bauer, Eva, additional, Blaas, Leander, additional, Hruschka, Natascha, additional, Zboray, Katalin, additional, Stiedl, Patricia, additional, Nivarthi, Harini, additional, Bogner, Edith, additional, Gruber, Wolfgang, additional, Mohr, Thomas, additional, Zwick, Ralf Harun, additional, Kenner, Lukas, additional, Poli, Valeria, additional, Aberger, Fritz, additional, Stoiber, Dagmar, additional, Egger, Gerda, additional, Esterbauer, Harald, additional, Zuber, Johannes, additional, Moriggl, Richard, additional, Eferl, Robert, additional, Győrffy, Balázs, additional, Penninger, Josef M., additional, Popper, Helmut, additional, and Casanova, Emilio, additional

Published
2015
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17. Adipocyte Glucocorticoid Receptor Deficiency Attenuates Aging- and HFD-Induced Obesity and Impairs the Feeding-Fasting Transition.

Author

Mueller, Kristina M., Hartmann, Kerstin, Kaltenecker, Doris, Vettorazzi, Sabine, Bauer, Mandy, Mauser, Lea, Amann, Sabine, Jall, Sigrid, Fischer, Katrin, Esterbauer, Harald, Müller, Timo D., Tschöp, Matthias H., Magnes, Christoph, Haybaeck, Johannes, Scherer, Thomas, Bordag, Natalie, Tuckermann, Jan P., and Moriggl, Richard

Subjects
*GLUCOCORTICOIDS, *ENERGY metabolism, *PATHOLOGICAL physiology, *METABOLOMICS, *OBESITY, *FAT cells, *ADIPOSE tissues, *AGING, *ANIMAL experimentation, *BETA adrenoceptors, *BIOCHEMISTRY, *HUMAN body composition, *CELL receptors, *CELLULAR signal transduction, *DIET, *FASTING, *FATTY liver, *FOOD habits, *GENETIC disorders, *HYPERTROPHY, *INSULIN, *LIPID metabolism disorders, *LIQUID chromatography, *LIVER, *MASS spectrometry, *MICE, *WESTERN immunoblotting
Abstract

Glucocorticoids (GCs) are important regulators of systemic energy metabolism, and aberrant GC action is linked to metabolic dysfunctions. Yet, the extent to which normal and pathophysiological energy metabolism depend on the GC receptor (GR) in adipocytes remains unclear. Here, we demonstrate that adipocyte GR deficiency in mice significantly impacts systemic metabolism in different energetic states. Plasma metabolomics and biochemical analyses revealed a marked global effect of GR deficiency on systemic metabolite abundance and, thus, substrate partitioning in fed and fasted states. This correlated with a decreased lipolytic capacity of GR-deficient adipocytes under postabsorptive and fasting conditions, resulting from impaired signal transduction from β-adrenergic receptors to adenylate cyclase. Upon prolonged fasting, the impaired lipolytic response resulted in abnormal substrate utilization and lean mass wasting. Conversely, GR deficiency attenuated aging-/diet-associated obesity, adipocyte hypertrophy, and liver steatosis. Systemic glucose tolerance was improved in obese GR-deficient mice, which was associated with increased insulin signaling in muscle and adipose tissue. We conclude that the GR in adipocytes exerts central but diverging roles in the regulation of metabolic homeostasis depending on the energetic state. The adipocyte GR is indispensable for the feeding-fasting transition but also promotes adiposity and associated metabolic disorders in fat-fed and aged mice. [ABSTRACT FROM AUTHOR]

Published
2017
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19. Impairment of Hepatic Growth Hormone and Glucocorticoid Receptor Signaling Causes Steatosis and Hepatocellular Carcinoma in Mice

Author

Mueller, Kristina M, Kornfeld, Jan-Wilhelm, Friedbichler, Katrin, Blaas, Leander, Egger, Gerda, Esterbauer, Harald, Hasselblatt, Peter, Schlederer, Michaela, Haindl, Susanne, Wagner, Kay-Uwe, Engblom, David, Haemmerle, Guenter, Kratky, Dagmar, Sexl, Veronika, Kenner, Lukas, Kozlov, Andrey V, Terracciano, Luigi, Zechner, Rudolf, Schuetz, Guenther, Casanova, Emilio, Pospisilik, J Andrew, Heim, Markus H, Moriggl, Richard, Mueller, Kristina M, Kornfeld, Jan-Wilhelm, Friedbichler, Katrin, Blaas, Leander, Egger, Gerda, Esterbauer, Harald, Hasselblatt, Peter, Schlederer, Michaela, Haindl, Susanne, Wagner, Kay-Uwe, Engblom, David, Haemmerle, Guenter, Kratky, Dagmar, Sexl, Veronika, Kenner, Lukas, Kozlov, Andrey V, Terracciano, Luigi, Zechner, Rudolf, Schuetz, Guenther, Casanova, Emilio, Pospisilik, J Andrew, Heim, Markus H, and Moriggl, Richard

Abstract

Growth hormone (GH)-activated signal transducer and activator of transcription 5 (STAT5) and the glucocorticoid (GC)-responsive glucocorticoid receptor (GR) are important signal integrators in the liver during metabolic and physiologic stress. Their deregulation has been implicated in the development of metabolic liver diseases, such as steatosis and progression to fibrosis. Using liver-specific STAT5 and GR knockout mice, we addressed their role in metabolism and liver cancer onset. STAT5 single and STAT5/GR double mutants developed steatosis, but only double-mutant mice progressed to liver cancer. Mechanistically, STAT5 deficiency led to the up-regulation of prolipogenic sterol regulatory element binding protein 1 (SREBP-1) and peroxisome proliferator activated receptor gamma (PPAR-gamma) signaling. Combined loss of STAT5/GR resulted in GH resistance and hypercortisolism. The combination of both induced expression of adipose tissue lipases, adipose tissue lipid mobilization, and lipid flux to the liver, thereby aggravating STAT5-dependent steatosis. The metabolic dysfunctions in STAT5/GR compound knockout animals led to the development of hepatic dysplasia at 9 months of age. At 12 months, 35% of STAT5/GR-deficient livers harbored dysplastic nodules and similar to 60% hepatocellular carcinomas (HCCs). HCC development was associated with GH and insulin resistance, enhanced tumor necrosis factor alpha (TNF-alpha) expression, high reactive oxygen species levels, and augmented liver and DNA damage parameters. Moreover, activation of the c-Jun N-terminal kinase 1 (JNK1) and STAT3 was prominent. Conclusion: Hepatic STAT5/GR signaling is crucial for the maintenance of systemic lipid homeostasis. Impairment of both signaling cascades causes severe metabolic liver disease and promotes spontaneous hepatic tumorigenesis., Funding Agencies|Austrian Science Funds (FWF)|SFB F28|FWF|SFB F30|Elise Richter fellowship (FWF)|V102-B12|grant GEN-AU Austromouse||Vienna Science and Technology Fund|LS07-058|JDRF

Published
2011
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20. Reply

Author

Mueller, Kristina M., primary and Moriggl, Richard, additional

Published
2013
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23. Erratum. Adipocyte Glucocorticoid Receptor Deficiency Attenuates Aging- and HFD-Induced Obesity and Impairs the Feeding-Fasting Transition. Diabetes 2017;66:272-286.

Author

Mueller, Kristina M, Hartmann, Kerstin, Kaltenecker, Doris, Vettorazzi, Sabine, Bauer, Mandy, Mauser, Lea, Amann, Sabine, Jall, Sigrid, Fischer, Katrin, Esterbauer, Harald, Müller, Timo D, Tschöp, Matthias H, Magnes, Christoph, Haybaeck, Johannes, Scherer, Thomas, Bordag, Natalie, Tuckermann, Jan P, and Moriggl, Richard

Subjects
*OBESITY treatment, *GLUCOCORTICOID receptors
Abstract

A correction to the article "Adipocyte Glucocorticoid Receptor Deficiency Attenuates Aging- and HFD-Induced Obesity and Impairs the Feeding-Fasting Transition" by M. Kristina et al. that was published in a 2017 issue of the journal "Diabetes" is presented.

Published
2018
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25. Reply: To PMID 21725989.

Author

Mueller KM and Moriggl R

Subjects
Animals, Male, Carcinoma, Hepatocellular metabolism, Fatty Liver metabolism, Growth Hormone metabolism, Liver Neoplasms metabolism, Receptors, Glucocorticoid metabolism, STAT5 Transcription Factor metabolism
Published
2013
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