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Whole genome microarray analysis of growth hormone induced genes in bone

ABSTRACT: Growth hormone (GH) is important in the development and maintenance of bone; however the IGF-dependent and -independent molecular pathways involved remain to be established. We used microarray analysis to identify genes acutely regulated by GH, in the bones of four week old GH-deficient mice at 6 or 24 hours following a single injection of GH (4 mg/kg body wt) or PBS (n = 6/group). 6,160 genes were differentially expressed at P = 0.05 and 17% of these genes were identified at both time points. Several of the 201 genes that were up or down regulated at > 2 fold at 6 and/or 24 hours (P = 0.01) were expressed sequence tags, transcription factors, or signaling genes. In conclusion, GH caused acute changes in several novel genes, suggesting that many GH-induced signaling pathways and target genes remain to be discovered Keywords: GH injection induced gene expression, time course

ORGANISM(S): Mus musculus

PROVIDER: GSE3689 | GEO | 2006/02/01

SECONDARY ACCESSION(S): PRJNA93835

REPOSITORIES: GEO

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Project description:The incidence of pre-diabetes (PD) and Type-2 Diabetes Mellitus (T2D) is a worldwide epidemic. African American (AA) individuals are disproportionately more likely to become diabetic than other ethnic groups. Over the long-term, metabolic complications related to diabetes result in significant alterations in growth hormone (GH) and insulin-like growth factor-1 (IGF-1). Considering the limited exercise-related studies in the area of gene expression changes with disease progression, the objective of this study was to examine differences in exercise-induced gene expression related to the GH and IGF-1 pathways in peripheral blood mononuclear cells (PBMCs) of healthy (CON) and PD AA individuals. Design: Ten subjects [5 PD (age=35±9.3 yr, BMI=32.1±4.0, FBG=101.8±1.3 mg/dl) and 5 CON (age=31±9.4 yr, BMI=29.4±5.2, FBG=82.8±9.7 mg/dl)] had blood drawn for RNA isolation prior to exercise (Pre), immediately following acute moderate intensity exercise on a treadmill (Post-1), 6-hours post (Post-6), and 24-hours post (Post-24). Isolation of mRNA from PBMCs was performed using ficoll separation, while the profiling of mRNA expression was performed using beadchip arrays that were scanned and analyzed by a gene expression module. Scan results were statistically analyzed for a specific list of genes related to GH and IGF-1. GH and IGF-1 protein levels were also assessed in each sample. To address issues of normality, all GH and IGF-1 data were log-transformed prior to analysis. Statistical significance was set at p<0.05. Results: Group differences for GH2 variant 2 (p=0.070) and GH2 variant 3 (p=0.059) were coupled with significant alterations in IGF-1 mRNA over time (p=0.024). A significant interaction between group and time was observed for GHRH mRNA (p=0.008). No group differences were observed in GH AUC (p=0.649), ∆GH (p=0.331), GHrec (p=0.294), or IGF-1 AUC (p=0.865), representing a similar exercise-induced GH and IGF-1 response for both groups. Conclusions: Analysis of GH and IGF-1 related-gene expression indicates that mild elevations in fasting blood glucose and exercise-induced alterations in gene expression are impacted by the prediabetic state.

Project description:E2 and GH are critical regulators of growth and intermediate metabolism in mammals. Hypothyroidism causes endocrine and metabolic disturbances in the liver with features that mimic deficiencies of E2 or GH signalling. In this work, we used the hypothyroid-orchiectomized (TXOX) adult rat model to evaluate the influence of E2 and GH on the liver in terms of global changes in gene expression. This study shows the changes in hepatic transcriptome that were provoked by E2 benzoate (50 ug/kg; sc; 5 days per week x 27 days), intermittent GH administration (0.3 mg/kg/day;sc injection divided into two daily injections x 7 days) or the combination of E2 plus GH in TXOX rats. E2 influenced the liver transcriptome, particularly genes involved in metabolism of lipids and endo-xenobiotics, and the GH-regulated endocrine, metabolic, gender, and immune responses. E2 did not prevent the inhibitory effects of GH on urea and amino acid metabolism-related genes. Notably, the combination of E2 and GH caused deleterious effects on transcriptional immune response. These results highlight the role of E2 as a critical regulator of liver metabolism in mammals and provide insights into the functional interplay between E2 and GH in the liver. Groups=4; Biological replicates = 4 per group; Samples=16; Reference samples=TXOX group. Adult (3 months old) male Sprague-Dawley rats (n=4 per group) were used throughout these experiments. The generation of TXOX was performed by adding methimazole (MMI; 0.05%) to the drinking water for 5 weeks starting on postnatal day (PND) 59 until sacrifice on PND94. Two weeks after starting MMI administration, male rats were castrated (OX) to make TXOX rats. Four days after OX, we began treatment with E2 benzoate (TXOXE2) or vehicle (TXOX) to TXOX rats for 20 days followed for 7 days by either vehicle plus GH (TXOXGH) or by E2 plus GH (TXOXE2GH). Twenty-four hours (in the case of E2) or twelve hours (in the case of GH) after the last injection, the animals were killed by exsanguinations. Portions of the liver were snap frozen in liquid nitrogen and stored at -80C until processed for mRNA analysis.

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Whole genome microarray analysis of growth hormone induced genes in bone

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