Induction of differentiation from hiPSCs into Leydig-like cells
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ABSTRACT:
PROVIDER: PRJNA1024913 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR26302223_1.fastq.gz | Fastqsanger.gz | |||
| SRR26302223_2.fastq.gz | Fastqsanger.gz | |||
| SRR26302224_1.fastq.gz | Fastqsanger.gz | |||
| SRR26302224_2.fastq.gz | Fastqsanger.gz | |||
| SRR26302225_1.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:Induction of differentiation from hiPSCs into Leydig-like cells (scRNA-Seq)
| PRJNA1028967 | ENA
Project description:We generated Leydig-like cells by the forced expression of NR5A1 in hiPSCs and by switching from 3D culture to adherent culture.
2025-01-07 | GSE244796 | GEO
Project description:We generated Leydig-like cells by the forced expression of NR5A1 in hiPSCs and by switching from 3D culture to adherent culture.
2025-01-07 | GSE245553 | 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. Fetal Leydig cells originate from proliferating progenitor cells in the gonadal interstitium, marked by genes like Arx, Pdgfra, Tcf21, Wnt5a, and Nr2f2. However, the precise mechanisms governing the transition from interstitial cells to Leydig cells remain elusive. Through integrated approaches involving animal models and multiomics, we have demonstrated that fetal Leydig cells originate from a Nr2f2 positive non-steroidogenic interstitial cell population. NR2F2 promotes progenitor cell fate while suppressing Leydig cell differentiation. Moreover, embryonic deletion of Nr2f2 in mouse testes resulted in disorders of sex development, including reduced testicular size, Leydig cell hypoplasia, cryptorchidism, and hypospadias. Collectively, our findings highlight the critical role of Nr2f2 in orchestrating the transition from interstitial cells to Leydig cells during testicular development.
2025-03-24 | GSE275901 | 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. Fetal Leydig cells originate from proliferating progenitor cells in the gonadal interstitium, marked by genes like Arx, Pdgfra, Tcf21, Wnt5a, and Nr2f2 (COUP-TFII). However, the precise mechanisms governing the transition from interstitial cells to Leydig cells remain elusive. Through integrated approaches involving animal models and multiomics, we have demonstrated that fetal Leydig cells originate from a COUP-TFII positive non-steroidogenic interstitial cell population. COUP-TFII promotes progenitor cell fate while suppressing Leydig cell differentiation. Moreover, embryonic deletion of COUP-TFII in mouse testes resulted in disorders of sex development, including reduced testicular size, Leydig cell hypoplasia, cryptorchidism, and hypospadias. Collectively, our findings highlight the critical role of COUP-TFII in orchestrating the transition from interstitial cells to Leydig cells during testicular development.
2025-03-24 | GSE275900 | 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:With the increasing common of reduced serum testosterone (T), or hypogonadism, in the male population, there is an urgent require for the approach of obtaining T-producing cells, which could be used to treat hypogonadism based on transplantation and reestablishment of T-producing cell lineage in the body. In human, T is mainly synthesized by the Leydig cells (LCs) that have been proposed to derive from mesenchymal cells of mesonephric origin. Although mesenchymal cells have been successfully induced into LCs, the limited source and possible trauma to donors hinders their wide applications in clinic therapies. Alternatively, human induced pluripotent stem cells (hiPSCs) that are highly expandable in cell culture and have the potential to differentiate into all somatic cell types become the emerging source of autologous cell therapies. In this study, we have successfully induced the differentiation of hiPSCs through mesoderm and early mesenchymal progenitors (EMPs) into either human Leydig cell-like cells (hLLCs) or human adrenal cell-like cells (hALCs) under different chemically defined culture systems. Factors that are critical for the normal development of LCs were added to both culture systems. hLLCs are expressed all steroidogenic genes and proteins that are important for T biosynthesis and are specific for LCs, synthesize T rather than cortisol (F), secret steroid hormones in response to db-cAMP and 22(R)-hydroxycholesterol, and display ultrastructural features resembling LCs. Differentially, hALCs synthesize F rather than T, and secret much less of steroid hormones than hLLCs. Thereafter, we performed microarray analyses to profile the whole gene expression pattern of hiPSCs and thier derivatives hLLCs and hALCs.
2019-10-04 | GSE127915 | GEO
Project description:Ad4BP/SF-1 is a transcription factor regulating gene expression related to steroidogenesis and energy metabolism. Previous studies have indicated that Ad4BP/SF-1 regulates fetal Leydig cell differentiation from progenitor cells. However, the underlying regulatory mechanisms remain unclear. Here, we reveal that Ad4BP/SF-1 directly regulates energy metabolisms in differentiated fetal Leydig cells through transcriptional upregulation.
2025-03-24 | GSE292012 | GEO
Project description:In males, Leydig cells are the main producers of testosterone and insulin-like 3, hormones which are both essential for sex differentiation and reproductive functions. Nuclear receptor chicken ovalbumin upstream promoter-transcription factors II (COUP-TFII) is expressed in the cells committed to give rise to the fully functional steroidogenic adult Leydig cells and has a major role in their function and differentiation. Up to date, only handful of COUP-TFII gene targets have been reported. A transcriptomic approach was used to identify additional genes affected by depletion of COUP-TFII in mouse MA-10 Leydig cell line.
2021-07-01 | GSE163283 | GEO
Project description:Testosterone production by Leydig cells is a tightly regulated process requiring synchronized expression of several steroidogenic genes by numerous transcription factors. Myocyte enhancer factor 2 (MEF2) is a transcription factor recently identified in somatic cells of the male gonad. In other tissues, MEF2 is an essential regulator of organogenesis and cell differentiation. So far in the testis, MEF2 was found to regulate Leydig cell steroidogenesis by controlling Nr4a1 and Star gene expression. To expand our understanding of the role of MEF2 in Leydig cells, we performed microarray analyses of MA-10 Leydig cells depleted in MEF2 and results were analyzed using the Partek and IPA softwares. Several genes were differentially expressed in MEF2-depleted Leydig cells and 15 were validated by qPCR. A large number of these genes are known to be involved in fertility, gonad morphology and steroidogenesis and include Pde8a, Por, Ahr, Bmal1, Cyp1a1, Cyp1b1, Map2k1, Tsc22d3, Nr0b2, Smad4, and Star, which were all downregulated in the absence of MEF2. In silico analyses revealed the presence of MEF2 binding sites within the first 2 kb upstream the transcription start site of the Por, Bmal1, and Nr0b2 promoters, which suggests a direct regulation by MEF2. Using transient transfections in MA-10 Leydig cells, siRNA knockdown, and a MEF2-Engrailed dominant negative, we found that MEF2 activates the Por, Bmal1 and Nr0b2 promoters and that this requires an intact MEF2 element. Our results identify novel target genes for MEF2 and define MEF2 as an important regulator of Leydig cell function and male reproduction. MA-10 Leydig cells were treated with siRNA MEF2A/2D (siRNA MEF2) or scrambled siRNA as control (siRNA Ctrl) 48h before total RNA extraction.
2015-04-12 | E-GEOD-64128 | biostudies-arrayexpress