Leydig Cells in Spermatogenesis-Deficient Testes Experience Stress, but Proliferate to Enhance Testosterone Synthesis I
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ABSTRACT:
PROVIDER: PRJNA1149808 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR30298544_1.fastq.gz | Fastqsanger.gz | |||
| SRR30298544_2.fastq.gz | Fastqsanger.gz | |||
| SRR30298545_1.fastq.gz | Fastqsanger.gz | |||
| SRR30298545_2.fastq.gz | Fastqsanger.gz | |||
| SRR30298546_1.fastq.gz | Fastqsanger.gz |
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Project description:Leydig Cells in Spermatogenesis-Deficient Testes Experience Stress, but Proliferate to Enhance Testosterone Synthesis II
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Project description:We investigated somatic cell dynamics in testicular tissue lacking spermatogenesis using model mice with testis-specific deletion of the histone H3 variant gene H3t. Leydig cells in testes lacking spermatogenesis led to increased testosterone synthesis that occurred alongside a high inflammatory response and oxidative stress.
2024-12-27 | GSE275209 | GEO
Project description:We investigated somatic cell dynamics in testicular tissue lacking spermatogenesis using model mice with testis-specific deletion of the histone H3 variant gene H3t. Leydig cells in testes lacking spermatogenesis led to increased testosterone synthesis that occurred alongside a high inflammatory response and oxidative stress.
2024-12-27 | GSE275210 | GEO
Project description:Evidence that persistent environmental pollutants may target the male reproductive system is increasing. The male reproductive system is regulated by secretion of testosterone by testicular Leydig cells, and perturbation of Leydig cells function may have ultimate consequences. 3-methylsulfonyl-DDE (3-MeSO2-DDE) is a potent adrenal toxicants formed from the persistent insecticide DDT. Although studies have revealed endocrine disruptive effect of 3-MeSO2-DDE, the underlying mechanisms at cellular level in steroidogenic Leydig cells remains to be established. The current study addresses the effect of 3-MeSO2-DDE viability, hormone production and proteome response of primary neonatal porcine Leydig cells. The AlamarBlue™ assay was used to evaluate cell viability. Solid phase radioimmunoassay was used to measure concentration of hormones produced by both unstimulated and luteinizing hormone (LH)-stimulated Leydig cells following 48 h exposure. Protein samples from Leydig cells exposed to a non-cytotoxic concentration of 3-MeSO2-DDE (10µM) were subjected to nano-LC-MS/MS and analyzed on a Q Exactive mass spectrometer and quantified using label-free quantitative algorithm. Gene Ontology (GO) and Ingenuity Pathway Analysis (IPA) were carried out for functional annotation and identification of protein interaction networks. 3-MeSO2-DDE regulated Leydig cell steroidogenesis differentially depending on cell culture condition. Whereas its effect on testosterone secretion at basal condition was stimulatory, the effect on LH-stimulated cells was inhibitory. From triplicate experiments, a total of 7540 proteins were identified in which the abundance of 87 proteins in unstimulated Leydig cells and 146 proteins in LH-stimulated Leydig cells were found to be significantly regulated in response to 3-MeSO2-DDE exposure. These proteins not only are the first reported in relation to 3-MeSO2-DDE exposure, but also display small number of proteins shared between culture conditions, suggesting the action of 3-MeSO2-DDE on several targeted pathways, including mitochondrial dysfunction, oxidative phosphorylation, EIF2-signaling, and glutathion-mediated detoxification. Further identification and characterization of these proteins and pathways may build our understanding to the molecular basis of 3-MeSO2-DDE induced endocrine disruption in Leydig cells.
2016-01-05 | PXD003165 | Pride
Project description:Bisphenol A (BPA), a prevalent endocrine disruptor, has been implicated in male reproductive dysfunction, particularly affecting Leydig cells (LCs), which are critical for testosterone production. Here, we explore the impact of BPA on m6A RNA methylation and its regulatory effects on autophagy and LC function. Utilizing both in vivo and in vitro models, we demonstrate that BPA exposure significantly reduces testosterone biosynthesis and upregulates m6A modification in LCs. The m6A 'writer' METTL3 and 'eraser' ALKBH5 were found to play a central role in regulating the m6A levels in Leydig cells upon BPA exposure, and manipulating m6A methylation level mitigates BPA-induced Leydig cell injury.
2025-01-22 | GSE275504 | GEO
Project description:Testicular fetal Leydig cells are specialized for androgen production during embryogenesis. Testosterone is essential for regulating sex differentiation, spermatogenesis, and fertility. Deficiencies in Leydig cell differentiation can lead to various disorders of sex development and male reproductive conditions, such as ambiguous genitalia, hypospadias, cryptorchidism, and infertility. Understanding the differentiation of fetal Leydig cells is essential for comprehending male sexual differentiation, reproductive health, and fertility.
2025-03-24 | GSE275902 | GEO
Project description:Analysis of Sertoli and Leydig cell “translatome” utilizing an in vivo ribosome tagging strategy (RiboTag) that allows a detailed and physiologically relevant characterization of the polysome-associated mRNAs in vivo. Although progress has been made in the identification of specific transcripts that are translated in Sertoli and Leydig cells and their response to hormones, efforts to expand these studies have been restricted by technical hurdles. Our analysis identified all previously characterized Leydig and Sertoli cell-specific markers and identified in a comprehensive manner novel markers of Leydig and Sertoli cells; the translational response of these two cell types to gonadotropins or testosterone was also investigated.
2013-04-06 | GSE45799 | GEO
Project description:Luteinising hormone (LH) is a key regulator of male fertility through its effects on testosterone secretion by Leydig cells. Mice in which the LH receptor is knocked out (LuRKO) show reduced testicular size, reduced testosterone, elevated serum LH, and a spermatogenic arrest that can be rescued by administration of testosterone. This study examines the onset of spermatogenic arrest in LuRKO males using transcriptional profiling of developing mutant and control testes. We also examine the initial stages of testosterone rescue of the phenotype, in order to identify key upstream regulators of testosterone-dependent spermatogenesis.
2009-12-14 | GSE19453 | GEO
Project description:Steroid hormones regulate essential physiological processes and inadequate levels are associated with various pathological conditions. In testosterone-producing Leydig cells, steroidogenesis is strongly stimulated by LH via its receptor leading to increased cAMP production and expression of the steroidogenic acute regulatory (STAR) protein, which is essential for the initiation of steroidogenesis. Leydig cell steroidogenesis then passively decreases following the rapid degradation of cAMP into AMP by phosphodiesterases. In this study, we show that AMP-activated protein kinase (AMPK) is activated following cAMP breakdown in MA-10 and MLTC-1 Leydig cells. Activated AMPK then actively inhibits cAMP-induced steroidogenesis by repressing the expression of key regulators of steroidogenesis including Star and Nr4a1. Similar results were obtained in Y-1 adrenal cells and in the constitutive steroidogenic cell line R2C. Our data identify AMPK as an active repressor of steroid hormone biosynthesis in steroidogenic cells that is essential to preserve cellular energy and prevent excess steroid production. Steroid hormones regulate essential physiological processes and inadequate levels are associated with various pathological conditions. In testosterone-producing Leydig cells, steroidogenesis is strongly stimulated by LH via its receptor leading to increased cAMP production and expression of the steroidogenic acute regulatory (STAR) protein, which is essential for the initiation of steroidogenesis. Leydig cell steroidogenesis then passively decreases following the rapid degradation of cAMP into AMP by phosphodiesterases. In this study, we show that AMP-activated protein kinase (AMPK) is activated following cAMP breakdown in MA-10 and MLTC-1 Leydig cells. Activated AMPK then actively inhibits cAMP-induced steroidogenesis by repressing the expression of key regulators of steroidogenesis including Star and Nr4a1. Similar results were obtained in Y-1 adrenal cells and in the constitutive steroidogenic cell line R2C. Our data identify AMPK as an active repressor of steroid hormone biosynthesis in steroidogenic cells that is essential to preserve cellular energy and prevent excess steroid production. MA-10 Leydig cells were treated with either DMSO (control), 10 uM forskolin or forskolin+Aicar (1 mM) for 1.5 h before total RNA extraction
2014-08-19 | E-GEOD-50118 | biostudies-arrayexpress
Project description:About 10% of couples of reproductive age worldwide suffer from infertility, with male factors accounting for about 50%, and testosterone is essential for male fertility, but the mechanisms behind the poor sperm quality and abnormally low blood testosterone levels in diabetic patients are unclear. In this study, we found that the peptide Apelin (APLN) significantly inhibited testosterone secretion from Leydig cells (LCs), which in turn led to decreased sperm quality. APLN was found to be localized to leydig cells in the testes of several diabetic mice, and its expression was significantly increased. The addition of APLN to mouse leydig cells decreased testosterone content and decreased the expression of genes related to testosterone synthesis, but the addition of ML221, an APLN receptor inhibitor, significantly increased the expression of testosterone synthesis genes. Injecting ML221 into diabetic mice significantly increased testosterone levels in the blood, increased sperm count as well as enhanced sperm motility and ultimately increased live birth rate of mice after in vitro fertilization. Proteomics revealed that ML221 significantly increased the expression of NR2F2 and further activated the transcription of testosterone synthesis genes. This study will further use mouse and cellular models to completely unravel the specific mechanisms by which APLN inhibits testosterone secretion and elucidate the causes of decreased sperm quality in diabetic patients. This study provides a new clinical target for the development of drugs to improve fertility in diabetic patients.
2025-02-24 | GSE289564 | GEO