Ontology highlight
ABSTRACT:
PROVIDER: PRJEB39694 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| CHH_project_NGS_data_only.vcf.gz | Vcf | |||
| CHH_project_NGS_data_only.vcf.gz.tbi | Vcf | |||
| CHH_project_Sanger_sequencing_data_only.vcf.gz | Vcf | |||
| CHH_project_Sanger_sequencing_data_only.vcf.gz.tbi | Vcf |
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Project description:During development, gonadotropin releasing hormone (GnRH) neurons are born in the nasal placode and migrate to the hypothalamus, where they position to regulate sexual reproduction. Defective GnRH neuron development may lead to GnRH deficiency (GD) which is characterized by absent or delayed puberty. Several GD causative genes have been identified so far, but half of the cases are still idiopathic. The identification of candidate genes is also hampered by the difficulty in isolating and studying GnRH neurons, which are small in number, develop in a short developmental window and lack specific markers. Gene expression profiles of GnRH neurons are lacking, as obtaining primary GnRH neurons is challenging and no reports on gene expression profiles during the whole developmental process of GnRH neurons are available. In this work, we obtained the transcriptomic profile of sorted GFP-positive and unsorted GFP-negative cells from Gnrh1-GFP rat embryos at three developmental stages, representing the initiation (embryonic day (E)14), the peak (E17) and the completion of GnRH neuronal migration (E20).
2023-02-28 | GSE174896 | GEO
Project description:During development, gonadotropin releasing hormone (GnRH) neurons are born in the nasal placode and migrate to the hypothalamus, where they position to regulate sexual reproduction. Defective GnRH neuron development may lead to GnRH deficiency (GD) which is characterized by absent or delayed puberty. Several GD causative genes have been identified so far, but half of the cases are still idiopathic. The identification of candidate genes is also hampered by the difficulty in isolating and studying GnRH neurons, which are small in number, develop in a short developmental window and lack specific markers. Immortalized murine cell lines have been developed in past years. Of interest, GT1-7 represent hypothalamic post-migratory neurons, whereas GN11 cells represent GnRH neurons blocked at an early stage of their migration. Here, we obtained the transcriptomic profile of Gn11 abnd GT1-7 cells, representing GnRH neurons at an immature and mature developmental stage, respectively.
2023-02-28 | GSE174902 | GEO
Project description:Affymetrix gene expression profiling in cumulus cells (CC) retrieved from patients undergoing GnRH agonists and GnRH antagonists IVF treatment. Oocytes from three different maturity stages were considered: metaphase I oocytes (MI), nonfertilized metaphase II (MII) oocytes (MII-NF) and MII oocytes developed to blactocyst stage embryo (MII-BL). From 4 GnRH agonist treated patients, CC MI, CC MII-NF and CC MII-BL samples were collected; from 5 GnRH agonist and 6 GnRH antagonist treated patients, CC MII-NF and CC MII-BL samples were collected; and from 2 GnRH agonist and 4 GnRH antagonist treated patients, CC MI and CC MII-BL were collected. Altogether, 10 CC MI, 15 CC MII-NF and 21 CC MII-BL were collected and considered for transcriptome analysis.
2013-09-13 | E-GEOD-34230 | biostudies-arrayexpress
Project description:Identifying the early gene program induced by GnRH would help understand how GnRH-activated signaling pathways modulate gonadotrope secretory response. We previously analyzed GnRH-induced early genes in LbT2 cells, however these lack GnRH self-potentiation, a physiological attribute of gonadotropes. To minimize cellular heterogeneity, rat primary pituitary cultures were enriched for gonadotropes by 40-60% using a sedimentation gradient. Given the limited number of gonadotropes, RNA was amplified prior to microarray analysis. Thirty-three genes were up-regulated 40 minutes after GnRH stimulation. Real-time PCR confirmed regulation of several transcripts including fosB, c-fos, egr-2 and rap1b, a small GTPase and member of the Ras family. GnRH stimulated rap1b gene expression in gonadotropes, measured by a sensitive single cell assay. Immunocytochemistry revealed increased Rap1 protein in GnRH-stimulated gonadotropes. These data establish rap1b as a novel gene rapidly induced by GnRH and a candidate to modulate gonadotropin secretion in rat gonadotropes. Primary rat gonadotrope cells were exposed to 10 nM GnRH for 40 min, then harvested and processed for RNA extraction using a Qiagen RNeasy mini kit (Qiagen, Valencia, CA). A total of 12 Affymetrix Rat Expression Array 230 v2.0, namely 6 GnRH-treated and 6 vehicle-treated samples, each containing 31,000 gene clusters, were used. Data analysis was performed by Affymetrix GeneChip Operating System (GCOS). A gene was considered to be up-regulated by GnRH if there is at least 50% concordance across multiple pairwise comparisons of GnRH- vs. vehicle-treated microarrays, and if the fold-change was at least 1.50.
2011-08-16 | E-GEOD-31399 | biostudies-arrayexpress
Project description:Administration of GnRH antagonist in IVF has several advantages. However, studies have shown that GnRH antagonist protocol cycles have lower implantation and clinical pregnancy rates than GnRH agonist long protocol cycles. Endometrial receptivity rather than embryo quality is thought to account for this phenomenon, however the mechanism is still largely unknown. This microarray analysed human endometrium during ‘implantation window phase’ between three groups: 1) untreated control, 2) GnRH agonist long protocol, and 3) GnRH antagonist protocol. The differential gene between groups uncovered the molecular mechanism occurred in endometrium affected by the intake of GnRH agonist or GnRH antagonist. Further study of these differential gene promises to find the reasons for lower endometrial receptivity in patients treated with GnRH antagonist and to improve the implantation rate in GnRH antagonist protocols in IVF.
2018-06-27 | GSE107914 | GEO
Project description:Hypothalamic gonadotropin-releasing hormone (GnRH) neurons lays the foundation for human development and reproduction, however, the critical cell populations and the entangled mechanisms underlying the development of human GnRH neurons remain poorly understood. Here, by utilizing our established human pluripotent stem cells-derived GnRH neuron model, we decoded the cellular heterogeneity and differentiation trajectories at the single-cell level. We found that a glutamatergic neuron population, which generated together with GnRH neurons, showed similar transcriptomic properties with olfactory sensory neuron and provided the migratory path for GnRH neurons. Through trajectory analysis, we identified a specific gene module activated along the GnRH neuron differentiation lineage, and we examined one of the transcription factors, DLX5, expression in human fetal GnRH neurons. Furthermore, we found that Wnt inhibition could increase DLX5 expression, and improve the GnRH neuron differentiation efficiency through promoting neurogenesis and switching the differentiation fates of neural progenitors into glutamatergic neurons/GnRH neurons. Our research comprehensively reveals the dynamic cell population transition and gene regulatory network during GnRH neuron differentiation.
2022-10-04 | GSE212901 | GEO
Project description:61 human HCCs were analyzed for genome-wide gene expression. Samples were collected at two sites in Germany, Heidelberg (HD) and Hannover (N). The Heidelberg Collection include 40 independent HCC: 19 liver resections and 17 explant liver specimen (4 not determined); median age at surgery was 57 years (range, 16-78), and the male/female ratio was 3:1. All diagnoses were confirmed by histological reevaluation, and use of the samples was approved by the local ethics committee. From 3 patients, two HCC nodules were included that previously showed different aCGH, indicating independent tumor development (tagged by _2). The underlying etiologies were HBV (n=8), HCV (n=9), alcohol (n=14), cryptogenic (n=11), genetic hemochromatosis (n=3), and Alpha-1 antitrypsin deficiency (n=2). The Hannover Collection include 21 HCC (HCC-Grad: G1-G3). Technical replicates were tagged with _B or _C differential genes expression in HCC liver (n=61) compared to control group (cell lines, n=3; normal liver tissue(NL), n=7). Technical replicates are indicated by _2.
2013-09-05 | E-GEOD-50579 | biostudies-arrayexpress
Project description:Hepatic stellate cells (HSCs) experience phenotypic transformation, from the quiescent phenotype to the activated one, after different etiologies of liver injury. Liver fibrosis is then occurred upon the activation of HSCs. miR-16 deficiency is identified to be an important characteristic of HSCs activation. We used Affymetrix rat 230 2.0 arrays (Affymetrix, Santa Clara, U.S.A.) to uncover the global alternations of transcriptome under miR-16 restoration.
2012-08-28 | GSE40381 | GEO