E-PROT-125
Ontology highlight
ABSTRACT:
PROVIDER: E-PROT-125 | ExpressionAtlas | 2024-02-20
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-PROT-125-MappedToGeneID.txt | Txt | |||
| E-PROT-125-MaxQuant_Summary_ExpressionAtlas.pdf | ||||
| E-PROT-125-analysis-methods.tsv | Tabular | |||
| E-PROT-125-configuration.xml | Xml | |||
| E-PROT-125-factors.xml | Xml |
Items per page: 5 1 - 5 of 12 |
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Project description:The liver is a central target organ of growth hormone (GH), which stimulates the synthesis of insulin-like growth factor 1 (IGF1) and affects multiple biochemical pathways. A systematic multi-omics analysis of GH actions in the liver has not been performed. GH receptor (GHR) deficiency is a unique model for studying consequences of lacking GH actions. In this study, we used molecular profiling techniques to capture a broad spectrum of these effects in the liver of a clinically relevant large animal model.
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Project description:Sex-dependent pituitary growth hormone (GH) secretory patterns determine the sex-biased expression of >1,000 genes in mouse and rat liver, affecting lipid and drug metabolism, inflammation and disease. A fundamental biological question is how robust differential expression can be achieved for hundreds of sex-biased genes simply based on the GH input signal pattern: pulsatile GH stimulation in males vs. near-continuous GH exposure in females. STAT5 is an essential transcriptional mediator of the sex-dependent effects of GH in the liver, but the mechanisms that underlie its sex-dependent actions are obscure. Here we elucidate the dynamic, sex-dependent binding of STAT5 and the GH/STAT5-regulated repressor BCL6 to mouse liver chromatin, revealing the counteractive interplay between these two regulators of liver sex-specificity. Our findings establish a close correlation between sex-dependent STAT5 binding and sex-biased target gene expression. Moreover, sex-dependent STAT5 binding correlated positively with sex-biased DNase hypersensitivity and H3-K4me1 and H3-K4me3 (activating) marks, correlated negatively with sex-biased H3-K27me3 (repressive) marks, and was associated with sex-differentially enriched motifs for HNF6/CDP factors. Importantly, BCL6 binding was preferentially associated with repression of female-biased STAT5 targets in male liver. Furthermore, BCL6 and STAT5 common targets but not BCL6 unique targets showed strong enrichment for lipid and drug metabolism. These findings provide a comprehensive, genome-wide view of the mechanisms whereby these two GH-regulated transcription factors establish and maintain sex differences affecting liver physiology and disease. The approaches used here to characterize sex-dependent STAT5 and BCL6 binding can be applied to other condition-specific regulatory factors and binding sites and their interplay with co-operative chromatin-binding factors. Mouse livers were excised from individual male and female mice killed at either a peak of STAT5 binding activity, or during the growth hormone (GH) interpulse interval, when STAT5 activity is either low (females) or essentially undetectable (males). Sonicated, cross-linked liver nuclear chromatin was then used to identify STAT5 binding sites by ChIP-Seq.
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Project description:Laron Syndrome (LS) is a rare hereditary disease in humans caused by a mutation in the growth hormone receptor gene which leads to high levels of circulating GH [1]. The disease is characterized by short statue, obesity, transient hypoglycemia during youth and low incidences of cancer and diabetes [2]. Thus making it interesting to study the underlying mechanisms. Recently a porcine model to mimic human LS was developed [3]. Growth hormone receptors are expressed on various cells of the immune system yet the extent to which dysregulation of GH might affect immune function in LS is poorly understood [4]. Therefore we decided to characterize the influence of growth hormone receptor knockout on the immune function of these animals by analyzing the proteome of their CD4+ and CD4- peripheral blood mononuclear cells (PBMC). 1. Werner, H.; Sarfstein, R.; et al. Laron Syndrome Research Paves the Way for New Insights in Oncological Investigation. Cells 2020, 9, doi:10.3390/cells9112446. 2. Werner, H.; Lapkina-Gendler, L.; et al. Genome-Wide Profiling of Laron Syndrome Patients Identifies Novel Cancer Protection Pathways. Cells 2019, 8, doi:10.3390/cells8060596. 3. Hinrichs, A.; Kessler, B.; et al. Growth hormone receptor-deficient pigs resemble the pathophysiology of human Laron syndrome and reveal altered activation of signaling cascades in the liver. Mol Metab 2018, 11, 113-128, doi:10.1016/j.molmet.2018.03.006. 4. Hattori, N. Expression, regulation and biological actions of growth hormone (GH) and ghrelin in the immune system. Growth Horm IGF Res 2009, 19, 187-197, doi:10.1016/j.ghir.2008.12.001.
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Project description:Effect of continuous GH treatment on old rat liver. Male rats, 2-year-old, were treated with vehicle or human GH (0.34 microgram/gram body weight) for 3 weeks. Keywords: response of old rat liver to growth hormone
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2014-12-01 | GSE56520 | GEO
Project description:Sex differences in liver gene expression are dictated by sex-differences in circulating growth hormone (GH) profiles. Presently, the pituitary hormone dependence of mouse liver gene expression was investigated on a global scale to discover sex-specific early GH response genes that might contribute to sex-specific regulation of downstream GH targets and to ascertain whether intrinsic sex-differences characterize hepatic responses to plasma GH stimulation. RNA expression analysis using 41,000-feature microarrays revealed two distinct classes of sex-specific mouse liver genes: genes subject to positive regulation (class-I) and genes subject to negative regulation by pituitary hormones (class-II). Genes activated or repressed in hypophysectomized (Hypox) mouse liver within 30-90min of GH pulse treatment at a physiological dose were identified as direct targets of GH action (early response genes). Intrinsic sex-differences in the GH responsiveness of a subset of these early response genes were observed. Notably, 45 male-specific genes, including five encoding transcriptional regulators that may mediate downstream sex-specific transcriptional responses, were rapidly induced by GH (within 30min) in Hypox male but not Hypox female mouse liver. The early GH response genes were enriched in 29 male-specific targets of the transcription factor Mef2, whose activation in hepatic stellate cells is associated with liver fibrosis leading to hepatocellular carcinoma, a male-predominant disease. Thus, the rapid activation by GH pulses of certain sex-specific genes is modulated by intrinsic sex-specific factors, which may be associated with prior hormone exposure (epigenetic mechanisms) or genetic factors that are pituitary-independent, and could contribute to sex-differences in predisposition to liver cancer or other hepatic pathophysiologies.
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Project description:We profiled the somatic landscape of 21 growth hormone (GH) -secreting pituitary adenomas using somatic copy-number alteration (SCNA), whole-genome sequencing (WGS), bisulfate sequencing, and transcriptome approaches. See details in Valimaki et al. Genetic and epigenetic characterization of growth hormone (GH) - secreting pituitary tumors. Manuscript in preparation, 2019.
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Project description:Individuals with hypopituitarism have an increased risk of developing non-alcoholic fatty liver disease (NAFLD)/non-alcoholic steatohepatitis (NASH) due to growth hormone (GH) deficiency. A rat model of hypopituitarism was established by hypophysectomy, followed by recombinant human growth hormone (rhGH) intervention. The mechanisms underlying GH deficiency-mediated NAFLD were elucidated through the application of label-free proteomics and phosphorylation proteomics.
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