Gene expression profile of the neonatal female mouse brain after administration of testosterone propionate.
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE59375 | GEO | 2015/07/31
SECONDARY ACCESSION(S): PRJNA255212
REPOSITORIES: GEO
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Project description:The aim of this study is to investigate the gene expression profiles during masculinization of neonatal female mice brain by exogenous androgen treatment. The results of our expression analysis will shed light on the identification of the key molecules of sexual differentiation of mammalian brain. Expression microarray analysis was performed using the RNAs extracted from the brains of neonatal mice treated with intraperitoneal injection of testosterone propionate during sex determination period of mice brain.
2015-07-31 | E-GEOD-59375 | biostudies-arrayexpress
Project description:Despite sharing much of their genomes, males and females are often highly dimorphic, reflecting at least in part the resolution of sexual conflict in response to sexually antagonistic selection. Sexual dimorphism arises owing to sex differences in gene expression, and steroid hormones are often invoked as a proximate cause of sexual dimorphism. Experimental elevation of androgens can lead to masculinization of behavior, physiology, and gene expression, but knowledge of the role of hormones remains incomplete, including how the sexes differ in their gene expression in response to exposure to hormones. We addressed these questions in a bird species with a long history of behavioral endocrinological and ecological study, the dark-eyed junco (Junco hyemalis), using a species-specific microarray. Focusing on two brain regions involved in sexually dimorphic behavior and regulation of hormone secretion, we identified 1,639 genes that differed in expression by sex in the ventromedial telencephalon and 768 in hypothalamus. In response to experimentally elevated testosterone, females exhibited a more “male-like” expression pattern than control females; unexpectedly, male expression patterns became more “female-like” rather than hyper-masculinized when compared to control males. This sex difference in pattern arose both because testosterone altered regulation of different genes in each sex and because testosterone altered regulation of the same genes differentially, i.e., up in one sex, down in the other. Hormonally regulated gene expression is a key genetic and physiological mechanism underlying sexual dimorphism, and further study should help to explain how it relates to the resolution of sexual conflict. Hypothalamus: 24 samples were analyzed, all were biological (not technical) replicates. 6 from males treated with testosterone [MT], 6 from control males [MC], 6 from females treated with testosterone [FT], and 6 from control females [FC]. All hybridizations were paired, and all treatment groups were compared, but no sample was analyzed more than once. Ventromedial telencephalon: 24 samples were analyzed, all were biological (not technical) replicates. 6 from males treated with testosterone [MT], 6 from control males [MC], 6 from females treated with testosterone [FT], and 6 from control females [FC]. All hybridizations were paired, and all treatment groups were compared, but no sample was analyzed more than once.
2013-01-30 | E-GEOD-41076 | biostudies-arrayexpress
Project description:Analysis of DNA methylation in the bed nucleus of the stria terminalis/preoptic area and striatum in response to perinatal testosterone exposure. The hypothesis tested was that treatment of females with testosterone on the day of birth would lead to masculinization of the methylome in adulthood. There were three experimental groups: males, females, and females treated with T on the day of birth. The methylation patterns in each group was determined using reduced representation bisulfite sequencing. Two brain regions and two time points (day 4 and day 60) were surveyed in each group. Each biological replicate is a pool of tissue from three animals.
2013-08-29 | E-GEOD-50218 | biostudies-arrayexpress
Project description:There has been growing interest in the relationship between maternal undernutrition and reproductive disorders in male offspring. In the present study, we determined the effects of maternal calorie restriction throughout the critical period for in utero development of the male reproductive system, termed the “masculinization programming window” on the reproductive system of mice. The intratesticular testosterone concentration of the fetuses of calorie-restricted (R) dams was lower than in control fetuses at 17.5 days post coitum. In addition, there was global down-regulation of genes encoding steroidogenic enzymes and a low sperm count in the offspring of R dams (R-offspring) at 6 weeks of age. Microarray analysis of the testes of the offspring identified dysregulation of several genes that might explain the derangement in spermatogenesis in the R-offspring. Thus, the present study provides insights into the impact of maternal undernutrition on the male reproductive system in mice. The deleterious effects probably originate in lower androgen exposure during the “masculinization programming window.”
2021-10-22 | GSE186345 | GEO
Project description:Our objective was to determine the nature and extent of androgen regulation of gene expression in the female lacrimal, meibomian,and submandibular glands, and to explore the degree to which this control is the same as in male glands. Keywords: Hormone treatment
2006-01-10 | GSE3995 | GEO
Project description:Analysis of DNA methylation in the bed nucleus of the stria terminalis/preoptic area and striatum in response to perinatal testosterone exposure. The hypothesis tested was that treatment of females with testosterone on the day of birth would lead to masculinization of the methylome in adulthood.
2013-08-29 | GSE50218 | GEO
Project description:BackgroundVolatile anesthetic exposure during development leads to long-term cognitive deficits in rats which are dependent on age and sex. Female rats are protected relative to male rats for the same exposure on postnatal day 7. Here we test our hypothesis that androgens can modulate chloride cotransporter expression to alter the susceptibility to neurotoxicity from GABAergic drugs using female rats with exogenous testosterone exposure.MethodsFemale rats were injected with testosterone (100 μg/animal) or vehicle on postnatal days 1 to 6. On postnatal day 7, the animals were randomized to either isoflurane exposure or sham. Spatial memory was assessed with the Barnes maze starting on postnatal day 41. Western blots were run from testosterone treated postnatal day 7 animals to measure levels of chloride cotransporters sodium-potassium-chloride symporter (NKCC1) and chloride-potassium symporter 5 (KCC2).ResultsExogenous testosterone modulated isoflurane anesthetic neurotoxicity in female rats based on poor performance in the probe trial of the Barnes Maze. By contrast, females with vehicle and isoflurane exposure were able to differentiate the goal position. These behavioral differences corresponded to differences in the protein levels of NKCC1 and KCC2 after exogenous testosterone exposure, with NKCC1 increasing ( P <0.001) and KCC2 decreasing ( P =0.003) relative to female controls.ConclusionsThe expression of chloride cotransporters, NKCC1 and KCC2, is altered by testosterone in female rats and corresponds to a cognitive deficit after isoflurane exposure. This confirms the role of androgens in perinatal anesthetic neurotoxicity and supports our hypothesis that the developing GABAergic system plays a critical role in the underlying mechanism.
| S-EPMC8671561 | biostudies-literature
Project description:Despite sharing much of their genomes, males and females are often highly dimorphic, reflecting at least in part the resolution of sexual conflict in response to sexually antagonistic selection. Sexual dimorphism arises owing to sex differences in gene expression, and steroid hormones are often invoked as a proximate cause of sexual dimorphism. Experimental elevation of androgens can lead to masculinization of behavior, physiology, and gene expression, but knowledge of the role of hormones remains incomplete, including how the sexes differ in their gene expression in response to exposure to hormones. We addressed these questions in a bird species with a long history of behavioral endocrinological and ecological study, the dark-eyed junco (Junco hyemalis), using a species-specific microarray. Focusing on two brain regions involved in sexually dimorphic behavior and regulation of hormone secretion, we identified 1,639 genes that differed in expression by sex in the ventromedial telencephalon and 768 in hypothalamus. In response to experimentally elevated testosterone, females exhibited a more “male-like” expression pattern than control females; unexpectedly, male expression patterns became more “female-like” rather than hyper-masculinized when compared to control males. This sex difference in pattern arose both because testosterone altered regulation of different genes in each sex and because testosterone altered regulation of the same genes differentially, i.e., up in one sex, down in the other. Hormonally regulated gene expression is a key genetic and physiological mechanism underlying sexual dimorphism, and further study should help to explain how it relates to the resolution of sexual conflict. Males and females can be highly dimorphic in metabolism and physiology despite sharing nearly identical genomes, and males and females both respond phenotypically to elevated testosterone, a steroid hormone that alters gene expression. Only recently has it become possible to learn how a hormone like testosterone affects global gene expression in non-model systems, and whether it affects the same genes in males and females. To investigate the transcriptional mechanisms by which testosterone exerts its metabolic and physiological effects on the periphery, we compared gene expression by sex and in response to experimentally elevated testosterone in a well-studied bird species, the dark-eyed junco (Junco hyemalis). We identified 324 genes in the liver, and 733 in the pectoralis muscle that were differentially expressed between males and females. In addition, we identified 1,872 genes that were differentially expressed between testosterone-treated and control individuals in at least one tissue and sex. Testosterone-treatment altered the expression of only130 genes in both males and females in the same tissue. These substantial differences in transcriptional response to testosterone suggest that males and females may employ different pathways when responding to elevated testosterone, despite the fact that many phenotypic effects of experimentally elevated testosterone are similar in the sexes. In contrast, of the 130 genes that were affected by testosterone-treatment in both sexes, 78% were regulated in the same direction (e.g. either higher or lower in testosterone-treated than control males and females). Thus, it appears that testosterone acts through both unique and shared transcriptional pathways in males and females, suggesting multiple mechanisms by which sexual conflict can be mediated.
2013-01-30 | GSE41076 | GEO
Project description:Abdominal aortic aneurysms (AAAs) exhibit marked sexual dimorphism with higher prevalence in men. Similarly, AAAs induced by angiotensin II (AngII) infusion into mice exhibit a higher prevalence in males. Testosterone promotes AAA pathology in adult male mice through regulation of angiotensin type 1A receptors (AT1aR) in abdominal aortas. However, mechanisms for sexual dimorphism of regional aortic angiotensin receptor expression and AAA formation are unknown.To define the role of developmental testosterone exposures in sexual dimorphism of AAAs, we determined if exposure of neonatal female mice to testosterone confers adult susceptibility to AngII-induced AAAs.One-day-old female hypercholesterolemic mice were administered a single dose of either vehicle or testosterone. Neonatal testosterone administration increased abdominal aortic AT1aR mRNA abundance and promoted a striking increase in AngII-induced AAAs in adult females exhibiting low serum testosterone concentrations. AngII-induced atherosclerosis and ascending aortic aneurysms were also increased by testosterone administration to neonatal females. In contrast, neonatal testosterone administration in males had no effect on AngII-induced vascular pathologies. Deficiency of AT1aR in smooth muscle cells reduced effects of neonatal testosterone to promote AAAs in adult females but did not alter atherosclerosis or ascending aortic aneurysms. Testosterone increased AT1aR mRNA abundance and hydrogen peroxide generation in cultured abdominal aortic SMCs. Increased AT1aR mRNA abundance was maintained during progressive passaging of female smooth muscle cells.These data reveal an unrecognized role of transient sex hormone exposures during neonatal development as long-lasting mediators of regional aortic AT1aR expression and sexual dimorphism of AAAs.
| S-EPMC3518797 | biostudies-literature
Project description:Androgenic steroids are increasingly used for hormone therapy of postmenopausal women and abused as life style drugs and for doping purposes, though knowledge about associated health risks in females is very limited. In order to understand more about short- and long-term androgen effects on a molecular level, we have analyzed hepatic gene expression in female C57BL/6 mice immediately after subcutaneous treatment with testosterone for 3 weeks and after 12 weeks hormone withdrawal using Affymetrix array technology and quantitative real-time RT-PCR. Among about 14,000 genes examined, 48 were up- and 65 genes were downregulated by testosterone after 3-weeks treatment and about 50% of these changes persisted even 12 weeks after testostrone withdrawal. In addition to obvious risks such as induction of hepatocellular carcinomas and virilization of liver metabolism, testosterone induced a series of changes, as e.g. dysregulation of hepatic gene expression due to incomplete conversion of female to male phenotype â in particular downregulation of cytochrom P450 isoforms and sulfotransferases. As a long-term testosterone effect, transcripts emerged in the liver that are normally specific for the exocine pancreas including amylase 2, ribonuclease 1, and several trypsin-, chymotrypsin-, and elastase-like proteases. This transdifferentiation of hepatic to exocrine pancreatic tissue indicates that testosterone can initiate long-lasting differentiation programs, which â once induced â progress even after androgen withdrawal. This may have far-reaching consequences difficult to foresee implying long-term hazards of testosterone-treatment for female health that have not been taken into account yet. Mice were treated with testosterone or sesame oil (vehicle) for three weeks twice a week. Gene expression in the liver was analyzed either directly after treatment or after three weeks of hormone/vehicle withdrawal. For each of these four groups, three individual mice were used as biological replicates.
2010-03-03 | E-GEOD-13388 | biostudies-arrayexpress