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Aging, inflammation and DNA damage in the somatic testicular niche with idiopathic germ cell aplasia

ABSTRACT: Aging, inflammation and DNA damage in the somatic testicular niche with idiopathic germ cell aplasia

PROVIDER: PRJNA646622 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12234210_1.fastq.gz	Fastqsanger.gz
	SRR12234210_2.fastq.gz	Fastqsanger.gz
	SRR12234211_1.fastq.gz	Fastqsanger.gz
	SRR12234211_2.fastq.gz	Fastqsanger.gz
	SRR12234212_1.fastq.gz	Fastqsanger.gz

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Aging, inflammation and DNA damage in the somatic testicular niche with idiopathic germ cell aplasia

Project description:Germ cell aplasia represents the most severe form of male infertility, and is associated with increased risk of early onset age-related chronic diseases and higher risk of death. Here we investigated the transcriptional landscape of 3880 somatic cells clustered in Sertoli, peritubular Myoid, Leydig, endothelial, stromal, T cells and macrophages from 3 human testis with idiopathic germ cell aplasia. Deregulated somatic pathways were associated with over-expression of paternally imprinted genes in immature Leydig cells, extracellular matrix composition and organization, hormonal milieu, chronic pro-inflammatory environments and early ageing, which were validated with an external cohort of 44 men with idiopathic germ cell aplasia compared to 102 age-matched fertile men. These 7 transcriptomic datasets unveil new insights into the germ cell aplasia, and prompts new thinking to better understand the pathogenesis of the idiopathic disease and the associated clinical manifestations of early ageing process.

2021-08-04 | GSE154535 | GEO

Protein composition of the extracellular matrix in idiopathic germ cell aplasia

Project description:The somatic microenvironment supports spermatogonial stem cell differentiation into sperm. Extracellular matrix (ECM) plays multiple roles in the stem cell niche, including self-renewal, proliferation, differentiation and survival of spermatogonial cells. The pathophysiology of male infertility might be representative of a progressive degenerative process of the testicular tissue, including ECM, rather than a defective genetic background, thus outlining the existence of chronic etiological agents/pathways. In this context, we sought to identify potential causative factors responsible for a number of modifications of the testicular somatic microenvironment associated with idiopathic germ cell aplasia in human beings. Proteomic analysis of the decellularized ECM was performed to study testis parenchyma from 10 idiopathic non-obstructive azoospermic (iNOA) men, dichotomized according to positive sperm retrieval versus germ cell aplasia. Germ cell aplasia was characterized by an increased nuclear distribution of the retinoic acid receptor in Sertoli cells which was associated with decreased expression of the ECM markers, Nidogen-2 and Heparan sulfate proteoglycan-2. Decreased levels of the interstitial matrisome associated Factor IX and its regulator VKORC1 were instead coupled with decreased signaling of vitamin K in Leydig cells. This study identified pathogenetic signature of the somatic testicular microenvironment and provide mechanistic insights into the molecular determinants of human idiopathic germ cell aplasia.

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Aging, inflammation and DNA damage in the somatic testicular niche with idiopathic germ cell aplasia.

Project description:Molecular mechanisms associated with human germ cell aplasia in infertile men remain undefined. Here we perform single-cell transcriptome profiling to highlight differentially expressed genes and pathways in each somatic cell type in testes of men with idiopathic germ cell aplasia. We identify immaturity of Leydig cells, chronic tissue inflammation, fibrosis, and senescence phenotype of the somatic cells, as well markers of chronic inflammation in the blood. We find that deregulated expression of parentally imprinted genes in myoid and immature Leydig cells, with relevant changes in the ratio of Lamin A/C transcripts and an active DNA damage response in Leydig and peritubular myoid cells are also indicative of senescence of the testicular niche. This study offers molecular insights into the pathogenesis of idiopathic germ cell aplasia.

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Project description:Pro-spermatogonia (SG) serve as the gateway to spermatogenesis. Using single-cell RNA sequencing (RNAseq), we studied the development of ProSG, their SG descendants, and testicular somatic cells, during the perinatal period in mice. We identified both gene and protein markers for 3 temporally distinct ProSG cell subsets, including a migratory cell population with a distinct transcriptome from the previously defined T1- and T2-ProSG stages. This intermediate (I)-ProSG subset translocates from the center of seminiferous tubules to the spermatogonial stem cell (SSC) “niche” in its periphery soon after birth. We identified 3 undifferentiated SG subsets at postnatal day 7, each of which express distinct genes, including transcription factor and signaling genes. Two of these subsets have the characteristics of newly emergent SSCs. We also molecularly defined the development of Sertoli, Leydig, and peritubular myoid cells during the perinatal period, allowing us to identify candidate signaling pathways acting between somatic and germ cells in a stage-specific manner during the perinatal period. Our study provides a rich resource for those investigating testicular germ and somatic cell developmental during the perinatal period.

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