Expression data from GT1-7 cells after treatment with GnRH
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ABSTRACT:
PROVIDER: PRJNA449335 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Analysis of GT1-7 cells treated with GnRH. In this dataset, we include the expression data obtained from GT1-7 cells after treatment with GnRH. We confirmed that GT1-7 cells expressed DUSP5 and DUSP6 after GnRH treatment. Results provide insight into the effect of GnRH on MAP kinase pathway.
2018-05-31 | GSE112857 | GEO
Project description:Arginine vasopressin (AVP) has been implicated in the regulation of gonadotropin-releasing hormone (GnRH) neurons, but the transcriptomic mechanisms underlying this effect remain unclear. In this study, GT1-7 GnRH neuronal cells were treated with AVP and analyzed by bulk RNA sequencing. Compared with control cells, AVP treatment induced broad transcriptional changes, with 1,094 differentially expressed genes identified, including 549 up-regulated and 545 down-regulated genes. Functional enrichment analysis highlighted AVP-associated changes in signaling pathways related to TNF signaling, PI3K-Akt signaling, MAPK signaling, cAMP signaling, axon guidance, and Wnt signaling. These data provide a transcriptomic resource for understanding AVP-responsive molecular programs in GT1-7 GnRH neurons.
2026-06-23 | GSE329856 | GEO
Project description:Based on previous experiments showing that Alisol B could regulate GnRH secretion from GT1-7 cells, cellular transcriptome sequencing was used to investigate the potential mechanism by which Alisol B regulates GnRH secretion from GT1-7 cells.
2025-04-12 | GSE253875 | 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:Stress is defined as a systemic nonspecific adaptive response to the stimulations from internal and external environment or psychological factors through coordinating series of complex systems, like nervous system, immune system and respiratory system. While it is well known that stress have profound negative effects on reproductive function, the mechanism of reproductive dysfunction is still far from perfect. Kisspeptin, which are known for regulating GnRH synthesis and secretion, affect the initiation of puberty and reproduction, have been shown to express glucocorticoid receptors(GR),and both acute and chronic stress significantly inhibit Kisspeptin expression. So, this study speculated that Kisspeptin might participate in the process of reproductive regulation during stress. However, when constructed stress models of GT1-7 cells(Derived from mouse hypothalamic neurons, could not only transcribe endogenous GnRH mRNA and release GnRH when depolarization, but also express Kisspeptin, G protein-coupled receptors) with DEX and tried to analyze the specific mechanism of stress inhibited Kisspeptin expression, opposite results(Dex improved Kisspeptin expression of GT1-7 cells) were obtained. Based on the neuroimmune system hypothesis of stress, this study speculated that the direct reason of stress inhibited Kisspeptin expression might be stress-induced inflammatory response rather than stress-elevated GC. Even so, the transcription of Il-1β decreased in BV-2 cells(Derived from mouse Microglia) after treated with DEX. Due to the proximity of Kisspeptin neurons and Microgila in arcuate nucleus(ARC) of hypothalamus, it is speculated that there maight be interaction between them. So, this study co-cultured GT1-7 cells and BV-2 cells, and found transcription of Kiss1 decreased and Il-1β increased. Decreased Kisspeptin expression due to inflammation of BV-2 cells and inflammation of BV-2 cells must due to changes of certain substances or molecules in GT1-7 cells after treated with DEX. To further explore the possible mechanism, this study used the highly sensitive miRNAs array to screen miRNAs which not only changed significantly in GT1-7 cells after treated with DEX but also associated with inflammation. Finally, 10 miRNAs obtained and further confirmed mmu-miR-146a-5P could inhibited the LPS-induced BV-2 cells inflammation, M1 polarization and apoptosis.
2025-12-31 | GSE230086 | GEO
Project description:Transcriptomic profiling reveals AVP-responsive molecular changes in GT1-7 GnRH neurons
| PRJNA1461951 | ENA
Project description:Expression data of immortlized GnRH neuron cell lines
| PRJNA731928 | ENA
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:Purpose: We sought a transcriptomic analysis of endometrial tissues following GnRH agonist treatment in a mouse model Methods: The neonatal female mice were randomly divided into three groups: control group, adenomyosis group and GnRH agonist treatment group. The pregnant outcome was observed and compared among the three groups. Besides, endometrial tissues from Day 4 of pregnancy were transcriptomic analysed using bioinformatics approaches. Results:We found that the litter size was smaller in adenomyosis group than control group (8±0.28vs. 11±0.26; P＜0.05).However, the average live litter size was increased (10±0.28 vs.8±0.28; P＜0.05) after GnRH agonist treatment. Transcriptomic analysis showed that compared with the adenomyosis group, 359 genes were differentially expressed in the GnRH agonist treatment group: 218 were down regulated and 141 were up regulated.Gene function analysis showed that the differentially expressed genes were related to diverse biological processes, including estrogen metabolism, cell cycle, and metabolites biosynthesis. Conclusions: GnRH agonist can improve the pregnancy outcome of adenomyosis in mouse model. Besides pituitary down regulation effect, other possible mechanisms may play role in GnRH agonist treatment, e.g., regulate cell proliferation cycle. It may be useful for the further understand the the mechanisms of the GnRH agonist in adeomyosis treatment.
2017-06-13 | GSE89463 | 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. 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