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RNA-Seq of testicular peritubular myoid cells, other testicular cells, and other tissue smooth muscle-like cells

ABSTRACT: In addition to germ cell population, testes contain several types of somatic cells, including Sertoli cells, Leydig cells, and peritubular myoid (PTM) cells. PTM cells are a type of smooth muscle-like cells and have contraction ability. To identify a marker of PTM cells, we isolated primary cells and subsequently performed RNA-Seq of testicular peritubular myoid cells (PTM_1, PTM_2, PTM_3), testicular Sertoli cells (Sertoli_1, Sertoli_2, Sertoli_3), testicular Leydig cells (Leydig_1, Leydig_2, Leydig_3), testicular germ cells (Germ_1, Germ_2, Germ_3), vascular smooth muscle cells (VSMC_1, VSMC_2, VSMC_3), intestinal smooth muscle cells (ISMC_1, ISMC_2, ISMC_3), and tracheal smooth muscle cells (TSMC_1, TSMC_2, TSMC_3) using BGISEQ-500 platform (BGI, China).

ORGANISM(S): Mus musculus

PROVIDER: GSE125303 | GEO | 2019/01/19

REPOSITORIES: GEO

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miRNA-Seq of testicular peritubular myoid cells, other testicular cells, and other tissue smooth muscle-like cells

Project description:In addition to germ cell population, testes contain several types of somatic cells, including Sertoli cells, Leydig cells, and peritubular myoid (PTM) cells. PTM cells are a type of smooth muscle-like cells and have contraction ability. To identify a marker of PTM cells, we isolated primary cells and subsequently performed miRNA-Seq of testicular peritubular myoid cells (PTM_1, PTM_2, PTM_3), testicular Sertoli cells (Sertoli_1, Sertoli_2, Sertoli_3), testicular Leydig cells (Leydig_1, Leydig_2, Leydig_3), testicular germ cells (Germ_1, Germ_2, Germ_3), vascular smooth muscle cells (VSMC_1, VSMC_2, VSMC_3), intestinal smooth muscle cells (ISMC_1, ISMC_2, ISMC_3), and tracheal smooth muscle cells (TSMC_1, TSMC_2, TSMC_3) using BGISEQ-500 platform (BGI, China).

2019-01-19 | GSE125302 | GEO

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Effect of endothelin-1 (ET-1) on mouse testicular peritubular myoid cells [RNA-Seq]

Project description:PTM cells can be induced to contract by endothelin 1 (ET1). We performed RNA-Seq of untreated testicular peritubular myoid cells (PTM_1, PTM_2, PTM_3) and ET1-treated peritubular myoid cells (ET1_1, ET1_2, ET1_3) using BGISEQ-500 platform (BGI, China).

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Effect of heat stress on mouse testicular peritubular myoid cells [RNA-seq]

Project description:We performed RNA-Seq of untreated testicular peritubular myoid cells (NC_1, NC_2, NC_3), and peritubular myoid cells that were collected 1 hour (H1_1, H1_2, H1_3) and 6 hours (H6_1, H6_2, H6_3) after heat treatment using BGISEQ-500 platform (BGI, China).

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Effect of heat stress on mouse testicular peritubular myoid cells [miRNA-seq]

Project description:We performed miRNA-Seq of untreated testicular peritubular myoid cells (NC_1, NC_2, NC_3), and peritubular myoid cells that were collected 1 hour (H1_1, H1_2, H1_3) and 6 hours (H6_1, H6_2, H6_3) after heat treatment using BGISEQ-500 platform (BGI, China).

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Project description:Peritubular cells of the human testis form a small compartment surrounding the seminiferous tubules. It contrast to rodents, it is composed of several cell layers and extracellular matrix. Peritubular cells are crucial for sperm transport and emerge as contributors to the spermatogonial stem cell niche, yet testicular peritubular cells are among the least known cell types of the human body. We employed single-cell RNA sequencing of cultured human testicular peritubular cells (HTPCs) isolated from testicular samples of donors with normal spermatogenesis and compared our data with recently published ex vivo data and, if available, with immunohistochemical data of the Human Protein Atlas. We observed a significant overlap between our results and genes expressed in vivo. Based on expression of a set of smooth muscle markers, HTPCs can be classified as smooth muscle cells. Small differences between in vivo/in vitro expressed genes may be due to plasticity/phenotypic switching. Plasticity was also shown upon addition of FCS to the culture medium. Based on transcriptome similarities four cellular states were observed. Characteristics of mesenchymal stromal cells and Leydig stem cells were noted, yet differentiation attempts into fat cells, bone cells or mature Leydig cells were not successful. Further analyses confirmed known stem cell niche-relevant factors (e.g. GDNF) and identified unknown functions e.g. the ability to produce retinoic acid. The results reveal that HTPCs upon isolation and culture are a highly adequate cellular model as they retain major characteristics. They therefore allow us to define the signature and functions of human testicular peritubular cells. The data may serve as a resource for future studies to better understand male (in)fertility.

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RNA-Seq of testicular peritubular myoid cells, other testicular cells, and other tissue smooth muscle-like cells

Project description:RNA-Seq of testicular peritubular myoid cells, other testicular cells, and other tissue smooth muscle-like cells

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miRNA-Seq of testicular peritubular myoid cells, other testicular cells, and other tissue smooth muscle-like cells

Project description:miRNA-Seq of testicular peritubular myoid cells, other testicular cells, and other tissue smooth muscle-like cells

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Leptin secreted from testicular microenvironment modulates hedgehog signaling to augment the endogenous function of Leydig cells

Project description:Although testosterone deficiency (TD) may be present in 1 out of 5 men 40 years or older, the factors responsible for TD remain largely unknown. Leydig stem cells (LSCs) differentiate into adult Leydig cells (ALC) and produce testosterone in the testes under the pulsatile control of luteinizing hormone (LH) from the pituitary gland. However, recent studies have suggested that the testicular microenvironment (TME), which is comprised of Sertoli and peritubular myoid cells (PMC), plays an instrumental role in LSC differentiation and testosterone production under the regulation of the desert hedgehog signaling pathway (DHH). It was hypothesized that TME releases paracrine factors to modulate LSC differentiation. For this purpose, cells (Sertoli, PMCs, LSCs and ALCs) were extracted from men undergoing testis biopsies for sperm retrieval and were evaluated for the paracrine factors in the presence or absence of TME (Sertoli and PMC). The results demonstrated that TME secretes leptin which induces LSC differentiation and increases T production. Leptin’s effects on LSC differentiation and T production, however, are inversely concentration-dependent: positive at low doses and negative at higher doses. Mechanistically, leptin acts on LSCs upstream of DHH; leptin-DHH regulation functions unidirectionally insofar as DHH gain or loss of function has no effects on leptin levels. Taken together, these findings identify leptin as a key paracrine factor released by cells within the TME that modulates LSC differentiation and testosterone release from mature Leydig cells, a finding with important clinical implications for TD.

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