Transcriptome profile of rat adrenal evoked by gonadectomy and testosterone or estradiol replacement
Ontology highlight
ABSTRACT:
ORGANISM(S): Rattus norvegicus
PROVIDER: GSE93726 | GEO | 2017/01/18
SECONDARY ACCESSION(S): PRJNA362207
REPOSITORIES: GEO
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Project description: Not available
| S-EPMC5309227 | biostudies-literature
Project description:We hypothesize that changes in adrenal gene expression mediate the increased plasma corticosterone and steroidogenesis in rat pups exposed to hypoxia from birth. Keywords: effects of hypoxia on adrenal steroidogenesis in the neonatal rat
2006-11-14 | GSE6249 | GEO
Project description:Transcription factor GATA6 is expressed in the fetal and adult adrenal cortex and has been implicated in steroidogenesis. To characterize the role of GATA6 in adrenocortical development and function, we generated mice in which Gata6 was conditionally deleted using Cre-LoxP recombination with Sf1-cre. The adrenal glands of adult Gata6 conditional knockout (cKO) mice were small and had a thin cortex with thickened capsule. Cytomegalic changes were evident in the adrenal glands of fetal and adult cKO mice, and chromaffin cells were ectopically located at the periphery of the glands. The secretion of corticosterone in response to exogenous ACTH was blunted in cKO mice. Cells expressing gonadal-like markers, including Gata4, Amhr2, and Tcf21, accumulated in the adrenal capsule and subcapsule of cKO mice, suggesting aberrant adrenocortical progenitor/stem cell differentiation. Gonadectomy triggered the overexpression of sex steroidogenic differentiation markers, such as Lhcgr and Cyp17, in the adrenal glands of male and female cKO mice. Nulliparous female and orchiectomized male cKO mice lacked an adrenal X-zone. Microarray hybridization identified Pik3c2g as a novel X-zone marker that is downregulated in the adrenal glands of nulliparous female Gata6 cKO mice. Our findings offer genetic proof of the longstanding hypothesis that GATA6 regulates the differentiation of steroidogenic progenitors into corticoid-producing cells. 3 replicates from both conditional knockout of Gata6 in the adrenal gland and control adrenal glands from non-knockout mice were compared
2013-06-06 | E-GEOD-40398 | biostudies-arrayexpress
Project description:We report that deletion of BMAL1 from adrenocortical cells using a SCC(Cyp11a1)-Cre driver reults in elevated plasma corticosterone in female, but not in male mice, following submaximal stress stimulation. RNA sequencing of adrenal glands from control and experimental animals was adopted to identify sex-dependent differences in gene expression that may explain the augmented corticosterone response specifically in female mice.
2019-04-13 | GSE129725 | GEO
Project description:Transcription factor GATA6 is expressed in the fetal and adult adrenal cortex and has been implicated in steroidogenesis. To characterize the role of GATA6 in adrenocortical development and function, we generated mice in which Gata6 was conditionally deleted using Cre-LoxP recombination with Sf1-cre. The adrenal glands of adult Gata6 conditional knockout (cKO) mice were small and had a thin cortex with thickened capsule. Cytomegalic changes were evident in the adrenal glands of fetal and adult cKO mice, and chromaffin cells were ectopically located at the periphery of the glands. The secretion of corticosterone in response to exogenous ACTH was blunted in cKO mice. Cells expressing gonadal-like markers, including Gata4, Amhr2, and Tcf21, accumulated in the adrenal capsule and subcapsule of cKO mice, suggesting aberrant adrenocortical progenitor/stem cell differentiation. Gonadectomy triggered the overexpression of sex steroidogenic differentiation markers, such as Lhcgr and Cyp17, in the adrenal glands of male and female cKO mice. Nulliparous female and orchiectomized male cKO mice lacked an adrenal X-zone. Microarray hybridization identified Pik3c2g as a novel X-zone marker that is downregulated in the adrenal glands of nulliparous female Gata6 cKO mice. Our findings offer genetic proof of the longstanding hypothesis that GATA6 regulates the differentiation of steroidogenic progenitors into corticoid-producing cells.
2013-06-06 | GSE40398 | GEO
Project description:We hypothesize that changes in adrenal gene expression mediate the increased plasma corticosterone and steroidogenesis in rat pups exposed to hypoxia from birth. Experiment Overall Design: In the current study, rat pups (with their dams) were exposed to hypoxia from birth and compared to pups from normoxic dams fed ad libitum. Adrenal glands were collected from normoxic and hypoxic pups at PD7and pooled (N=24/sample; 4 samples per treatment group) for total RNA extraction. Microarray analysis was performed, followed by verification with real-time PCR. Furthermore, the expression of selected genes involved in adrenal function was analyzed by real-time PCR, regardless of microarray results.
2008-06-14 | E-GEOD-6249 | biostudies-arrayexpress
Project description:We explored sex-biased effects of the primary stress glucocorticoid hormone corticosterone on the miRNA expression profile in the rat hippocampus. Adult adrenalectomized (ADX) female and male rats received a single corticosterone (10 mg/kg) or vehicle injection and after 6 h, hippocampi were collected for miRNA, mRNA and Western blot analyses. miRNA profiling microarrays showed a basal sex-biased miRNA profile in ADX rat hippocampi. Additionally, acute corticosterone administration triggered a sex-biased differential expression of miRNAs derived from genes located in several chromosomes and clusters on the X and 6 chromosomes. Putative promoter analysis unveiled that most corticosterone-responsive miRNA genes contained motifs for either direct or indirect glucocorticoid actions in both sexes. The evaluation of transcription factors indicated that almost 50 % of miRNA genes sensitive to corticosterone in both sexes was under glucocorticoid receptor regulation. Transcription factor-miRNA regulatory network analyses identified several transcription factors that regulate, activate or repress miRNA expression. Validated target mRNA analysis of corticosterone-responsive miRNAs showed a more complex miRNA-mRNA interaction network in males compared to females. Enrichment analysis revealed that several hippocampal-relevant pathways were affected in both sexes, such as neurogenesis and neurotrophin signaling. The evaluation of selected miRNA targets from these pathways displayed a strong sex difference in the hippocampus of ADX-vehicle rats. Corticosterone treatment did not change the levels of the miRNA targets and their corresponding tested proteins. Our data indicate that corticosterone exerts a sex-biased effect on hippocampal miRNA expression, which may engage in sculpting the basal sex differences observed at higher levels of hippocampal functioning.
2021-08-01 | GSE181268 | GEO
Project description:Gonadectomy (GDX) induces sex steroid-producing adrenocortical tumors in certain mouse strains and in the domestic ferret. Complementary approaches, including DNA methylation mapping and microarray expression profiling, were used to identify novel genetic and epigenetic markers of GDX-induced adrenocortical neoplasia in female DBA/2J mice. Markers were validated by quantitative RT-PCR, laser capture microdissection, in situ hybridization, and immunohistochemistry. Two genes with hypomethylated promoters, Igfbp6 and Foxs1, were upregulated in post-GDX adrenocortical neoplasms. The neoplastic cells also exhibited hypomethylation of the fetal adrenal enhancer of Sf1, an epigenetic signature that typifies descendants of fetal adrenal rather than gonadal cells. Expression profiling demonstrated upregulation of gonadal-like genes, including Spinlw1, Insl3, and Foxl2, in GDX-induced adrenocortical tumors of the mouse. One of these markers, FOXL2, was detected in adrenocortical tumor specimens from gonadectomized ferrets. These new markers may prove useful for studies of steroidogenic cell development and for diagnostic testing. Total RNA extracted from whole adrenal glands of gonadectomized and non-gonadectomized mice.
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Project description:Previous work has suggested that the hormones testosterone and corticosterone influence the process of meiotic segregation in the ovarian follicles of laying hens, ultimately influencing whether the resulting egg produces a male or female chick. We tested whether treatment with testosterone and/or corticosterone stimulated changes in the expression of genes that may influence the process of meiotic segregation as a next step towards understanding the mechanism by which these hormones may play a role in sex ratio adjustment in birds.
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Project description:Gonadectomy (GDX) induces sex steroid-producing adrenocortical tumors in certain mouse strains and in the domestic ferret. Complementary approaches, including DNA methylation mapping and microarray expression profiling, were used to identify novel genetic and epigenetic markers of GDX-induced adrenocortical neoplasia in female DBA/2J mice. Markers were validated by quantitative RT-PCR, laser capture microdissection, in situ hybridization, and immunohistochemistry. Two genes with hypomethylated promoters, Igfbp6 and Foxs1, were upregulated in post-GDX adrenocortical neoplasms. The neoplastic cells also exhibited hypomethylation of the fetal adrenal enhancer of Sf1, an epigenetic signature that typifies descendants of fetal adrenal rather than gonadal cells. Expression profiling demonstrated upregulation of gonadal-like genes, including Spinlw1, Insl3, and Foxl2, in GDX-induced adrenocortical tumors of the mouse. One of these markers, FOXL2, was detected in adrenocortical tumor specimens from gonadectomized ferrets. These new markers may prove useful for studies of steroidogenic cell development and for diagnostic testing.
2014-07-31 | GSE54393 | GEO