Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA341957 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Genes and mechanisms regulated by androgens as possible contributors to the male excess observed in autism
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Project description:Genes and mechanisms regulated by androgens as possible contributors to the male excess observed in autism [LNCaP]
| PRJNA341958 | ENA
Project description:Genes and pathways regulated by androgens as possible contributors to the male excess observed in autism [RNA-Seq]
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Project description:We analyzed androgens effects on human neural stem cells (hNSCs) by RNA-sequencing after either DMSO (solvent), DHT 100nM, 10nM, Testosterone 100nM, 10nM, R1881 1nM or retinoic acid 1µM 24 hours treatment in order to find the role of androgen receptor (AR) during brain development.
2018-02-01 | GSE86457 | GEO
Project description:Autism spectrum disorder (ASD) is a highly heterogeneous neurodevelopmental disorder that significantly jeopardizes the physical and mental well-being of children. Autism spectrum disorder results from a combination of environmental and genetic factors. Hyperandrogenic exposure during pregnancy increases their risk of developing autism. Nevertheless, the prenatal exposure to androgens affects offspring neurodevelopment and the underlying mechanisms have not been fully elucidated. In the present study, administration of excessive dihydrotestosterone (DHT) to pregnant mice was found to impair neuronal development and dendritic spine formation in offspring, inducing autism-like behaviors. Furthermore, through mRNA transcriptome sequencing technology, the key molecule Nr4a2 was identified during this process of change. Overexpression of Nr4a2 and treatment with amodiaquine (AQ) significantly improved the abnormal phenotypes in offspring caused by prenatal exposure to androgens. Overall, Nr4a2 emerges as a crucial molecule involved in the impairment of offspring neurodevelopment due to prenatal androgen exposure, which provides a new perspective for the in-depth study of the influencing factors and underlying mechanisms.
2023-11-04 | GSE246534 | GEO
Project description:Male sex predispose to many kidney diseases. Considering that androgens exert deleterious effects in a variety of cell types within kidney, we hypothesized that dihydrotestosterone (DHT) would impair the biology of the renal tubular cell by inducing changes in the proteome. We employed stable isotope labeling with amino acids (SILAC) in an indirect spike-in fashion to accurately quantify the proteome in DHT- and 17β-estradiol (EST)-treated human proximal tubular epithelial cells (PTEC), in 4 different experiments. Of the 5043 quantified proteins, 76 were differentially regulated. Biological processes related to energy metabolism were significantly enriched among DHT-regulated proteins. SILAC ratios of 3 candidates representing glycolysis, N-acetylglucosamine metabolism and fatty acid β-oxidation, namely glucose-6-phosphate isomerase (GPI), glucosamine-6-phosphate-N-acetyltransferase 1 (GNPNAT1) and mitochondrial trifunctional protein subunit alpha (HADHA), were verified in vitro. In vivo, renal GPI and HADHA protein expression was increased in males. Furthermore, male sex was associated to higher GPI, GNPNAT1 and HADHA protein expression in diabetic Akita mice. Functional group enrichment analysis revealed a link between our DHT-regulated proteins and glycosphingolipid metabolism within the male kidney. This is the most in depth quantitative proteomic study of human primary PTEC response to sex hormone treatment. In this study we open new perspectives on how to explore the molecular mechanisms responsible for the deleterious effects of androgens in the context of kidney disease, especially diabetic nephropathy.
2017-01-17 | PXD003811 | Pride
Project description:Male sex predispose to many kidney diseases. Considering that androgens exert deleterious effects in a variety of cell types within kidney, we hypothesized that dihydrotestosterone (DHT) would impair the biology of the renal tubular cell by inducing changes in the proteome. We employed stable isotope labeling with amino acids (SILAC) in an indirect spike-in fashion to accurately quantify the proteome in DHT- and 17?-estradiol (EST)-treated human proximal tubular epithelial cells (PTEC), in 4 different experiments. Of the 5043 quantified proteins, 76 were differentially regulated. Biological processes related to energy metabolism were significantly enriched among DHT-regulated proteins. SILAC ratios of 3 candidates representing glycolysis, N-acetylglucosamine metabolism and fatty acid ?-oxidation, namely glucose-6-phosphate isomerase (GPI), glucosamine-6-phosphate-N-acetyltransferase 1 (GNPNAT1) and mitochondrial trifunctional protein subunit alpha (HADHA), were verified in vitro. In vivo, renal GPI and HADHA protein expression was increased in males. Furthermore, male sex was associated to higher GPI, GNPNAT1 and HADHA protein expression in diabetic Akita mice. Functional group enrichment analysis revealed a link between our DHT-regulated proteins and glycosphingolipid metabolism within the male kidney. This is the most in depth quantitative proteomic study of human primary PTEC response to sex hormone treatment. In this study we open new perspectives on how to explore the molecular mechanisms responsible for the deleterious effects of androgens in the context of kidney disease, especially diabetic nephropathy.
2017-03-31 | MSV000080854 | MassIVE
Project description:Neuroprotective, anti-inflammatory and remyelinating properties of androgens are well-characterized in demyelinated male mice and men suffering from multiple sclerosis. However, androgen effects mediated by the androgen receptor AR, have been only poorly studied in females who make low androgen levels. Here, we show a predominant microglial AR expression in demyelinated lesions from female mice and women with multiple sclerosis, but virtually undetectable AR expression in lesions from male animals and men with multiple sclerosis. In female mice, androgens and estrogens act in a synergistic way while androgens drive microglia response towards regeneration. Transcriptomic comparisons of demyelinated mouse spinal cords indicate that, regardless of the sex, androgens up-regulate genes related to neuronal function integrity and myelin production. Depending on the sex, androgens down-regulate genes related to the immune system in females and lipid catabolism in males. Thus, androgens are required for proper myelin regeneration in females and therapeutic approaches of demyelinating diseases need to consider male-female differences.
2023-02-19 | GSE225254 | GEO
Project description:TCQA promoted differentiation of hNSCs at least toward the neuronal lineage and suggests the possibility of using TCQA to promote neurogenesis. When differentiation is induced by growth factor withdrawal, decreased expression of stemness gene and increased expression of NSC fate-promoting genes can be observed. Therefore, we evaluated the effect of TCQA on global gene expression in hNSCs during differentiation at 24h to elucidate the neurogenesis-promoting effects of TCQA.
2023-07-03 | GSE235835 | GEO
Project description:Epiphycan/Biglycan double-null mice develop age-dependant osteoarthritis. This study aims to elucidate the gene expression changes which happen early in the disease (3 Months) in order to identify possible contributors to disease devleopment and progression. Note: CEL files for GSM230344 and GSM230347 are not available Experiment Overall Design: Two wildtype and three epiphycan/biglycan-null arrays were performed using Affymetrix Genechip technology. For each chip, the tibio-femoral joints of three male mice (6 joints per sample) were pooled and RNA extracted, labeled, and hybridized.
2008-04-05 | E-GEOD-9099 | biostudies-arrayexpress