Gene expression of transgenic knock-in mutant growth hormone receptor mice
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE11396 | GEO | 2009/02/01
SECONDARY ACCESSION(S): PRJNA106521
REPOSITORIES: GEO
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Project description:Numerous genetic manipulations that extend lifespan in mice have been discovered over the past two decades, the most robust of which has arguably been the down regulation of growth hormone (GH) signaling. However, while decreased GH signaling has been associated with improved health and lifespan, many of the underlying physiological changes and molecular mechanisms have yet to be elucidated. To this end, we have completed the first transcriptomic and metabolomic study on long-lived growth hormone releasing hormone knockout (GHRH-KO) and wild-type mice in brown adipose tissue (transcriptomics) and blood serum (metabolomics). We find that GHRH-KO mice have increased transcript levels of mitochondrial and amino acid genes with decreased levels of extracellular matrix genes. Concurrently, mitochondrial metabolites are differentially regulated in GHRH-KO. Furthermore, we find a strong signal of genotype-by-sex interactions, suggesting the sexes have differing physiological responses to GH deficiency. Overall, our results point towards a strong influence of mitochondrial metabolism in GHRH-KO mice which potentially is tightly intertwined with their extended lifespan phenotype.
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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:Mice with disruptions of growth hormone-releasing hormone (GHRH) or growth hormone receptor (GHR) exhibit similar phenotypes of prolonged lifespan and delayed age-related diseases. However, these two models respond differently to calorie restriction indicating that they might carry different and/or independent mechanisms for improved longevity and healthspan. In order to elucidate these mechanisms, we generated GHRH and GHR double-knockout mice (D-KO). In the present study, we focused specifically on the characteristics of female D-KO mice. The D-KO mice have reduced body weight and enhanced insulin sensitivity compared to wild-type (WT) controls. Growth retardation in D-KO mice is accompanied by decreased GH expression in pituitary, decreased circulating IGF-1, increased high-molecular-weight (HMW) adiponectin, and leptin hormones compared to WT controls. Generalized linear model-based regression analysis, which controls for body weight differences between D-KO and WT groups, shows that D-KO mice have decreased lean mass, bone mineral density, and bone mineral content, but increased adiposity. Indirect calorimetry markers including oxygen consumption, carbon dioxide production, and energy expenditure were significantly lower in D-KO mice relative to the controls. In comparison with WT mice, the D-KO mice displayed reduced respiratory exchange ratio (RER) values only during the light cycle, suggesting a circadian-related metabolic shift toward fat utilization. Interestingly, to date survival data suggest extended lifespan in D-KO female mice.
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