MiRNA profiling of human Sertoli cells-derived extracellular vesicles
Ontology highlight
ABSTRACT:
ORGANISM(S): synthetic construct Homo sapiens
PROVIDER: GSE192696 | GEO | 2021/12/28
REPOSITORIES: GEO
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Project description:We performed a proteomic analysis of EVs derived from human Sertoli cells, aiming to obtain the profiling of the proteins in these EVs to explore their possible roles in the development of testis.
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Project description:Although decades of research have established that androgen is essential for spermatogenesis, androgen’s mechanism of action remains elusive. This is in part because only a few androgen-responsive genes have been definitively identified in the testis. Here, we report that microRNAs—small, noncoding RNAs—are one class of androgen-regulated trans-acting factors in the testis. Specifically, by using androgen suppression and androgen replacement in mice, we show that androgen regulates the expression of several microRNAs in Sertoli cells. Our results reveal that several of these microRNAs are preferentially expressed in the testis and regulate genes that are highly expressed in Sertoli cells. Because androgen receptor–mediated signaling is essential for the pre- and postmeiotic germ cell development, we propose that androgen controls these events by regulating Sertoli/germ cell–specific gene expression in a microRNA-dependent manner.
2012-12-21 | GSE37679 | GEO
Project description:Although decades of research have established that androgen is essential for spermatogenesis, androgen’s mechanism of action remains elusive. This is in part because only a few androgen-responsive genes have been definitively identified in the testis. Here, we report that microRNAs—small, noncoding RNAs—are one class of androgen-regulated trans-acting factors in the testis. Specifically, by using androgen suppression and androgen replacement in mice, we show that androgen regulates the expression of several microRNAs in Sertoli cells. Our results reveal that several of these microRNAs are preferentially expressed in the testis and regulate genes that are highly expressed in Sertoli cells. Because androgen receptor–mediated signaling is essential for the pre- and postmeiotic germ cell development, we propose that androgen controls these events by regulating Sertoli/germ cell–specific gene expression in a microRNA-dependent manner. Control, Treated, Rescued (3 groups)
2012-12-21 | E-GEOD-37679 | biostudies-arrayexpress
Project description:Malignant germ-cell-tumours (GCTs) are characterised by microRNA (miRNA/miR-) dysregulation, with universal over-expression of miR-371~373 and miR-302/367 clusters regardless of patient age, tumour site, or subtype (seminoma/yolk-sac-tumour/embryonal carcinoma). These miRNAs are released into the bloodstream, presumed within extracellular-vesicles (EVs) and represent promising biomarkers. Here, we comprehensively examined the role of EVs, and their miRNA cargo, on (fibroblast/endothelial/macrophage) cells representative of the testicular GCT (TGCT) tumour microenvironment (TME). Small RNA next-generation-sequencing was performed on 34 samples, comprising representative malignant GCT cell lines/EVs and controls (testis fibroblast [Hs1.Tes] cell-line/EVs and testis/ovary samples). TME cells received TGCT co-culture, TGCT-derived EVs, and a miRNA overexpression system (miR-371a-OE) to assess functional relevance. TGCT cells secreted EVs into culture media. MiR-371~373 and miR-302/367 cluster miRNAs were overexpressed in all TGCT cells/subtypes compared with control cells and were highly abundant in TGCT-derived EVs, with miR-371a-3p/miR-371a-5p the most abundant. TGCT co-culture resulted in increased levels of miRNAs from the miR-371~373 and miR-302/367 clusters in TME (fibroblast) cells. Next, fluorescent labelling demonstrated TGCT-derived EVs were internalised by all TME (fibroblast/endothelial/macrophage) cells. TME (fibroblast/endothelial) cell treatment with EVs derived from different TGCT subtypes resulted in increased miR-371~373 and miR-302/367 miRNA levels, and other generic (eg, miR-205-5p/miR-148-3p) and subtype-specific (seminoma, eg, miR-203a-3p; yolk-sac-tumour, eg, miR-375-3p) miRNAs. MiR-371a-OE in TME cells resulted in increased collagen contraction (fibroblasts) and angiogenesis (endothelial cells), via direct mRNA downregulation and alteration of relevant pathways. TGCT cells communicate with nontumour stromal TME cells through release of EVs enriched in oncogenic miRNAs, potentially contributing to tumour progression.
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Project description:To elucidate the role(s) of WNT/CTNNB1 signaling in the testis, transgenic Ctnnb1 tm1Mmt/+;Amhr2 tm3(cre)Bhr/+ mice were generated to obtain sustained activation of the WNT/CTNNB1 pathway in Sertoli cells. Male Ctnnb1 tm1Mmt/+;Amhr2 tm3(cre)Bhr/+ mice were sterile because of testicular atrophy starting at 5 wk of age, associated with degeneration of seminiferous tubules and the progressive loss of germ cells. Sustained WNT/CTNNB1 pathway activation was obtained in Ctnnb1 tm1Mmt/+;Amhr2 tm3(cre)Bhr/+ Sertoli cells. Sertoli cells often exhibited morphological characteristics suggestive of incomplete differentiation that appeared in a manner coincident with germ cell loss, accompanied by an increase in the expression of the immature Sertoli cell marker AMH. Microarray analyses performed on cultured Sertoli cells showed that CTNNB1 induces the expression of genes associated with the female sex determination pathway as well as cell-cycle associated genes . Together, these data suggest that the WNT/CTNNB1 pathway regulates Sertoli cell functions critical to their capacity to support spermatogenesis and to proliferate in the postnatal testis.
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Project description:To compare the transcriptional profile of endogenous Sertoli cells from different Stage of Sertoli cell development (embryonic, immature, mature) to the transcriptionla profile of induced embryonic Sertoli cells derived from MEFs or TTFs we employed the agilent whole genome microarray Keywords: Expression profiling by array The following samples were analyzed in duplicates (MEFs, TTFs, ieSCs (derived from MEFs), ieSCs (derived from TTFs), 14.5 dpc male gonad, immature Sertoli (19 dpc embryo testis) and mature (8 week-old mouse testis))
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Project description:Elevated palmitic acid, a most abundant saturated fatty acid, is a risk factor for obesity complications. Here, we report that palmitic acid impairs spermatogenesis by inducing abnormal palmitoylation in Sertoli cells. Firstly, we proposed a correlation between palmitic acid and spermatogenesis by reporting a significant elevation of serum palmitic acid levels in patients with dyszoospermia. In palmitic acid -treated mice, the blood-testis barrier was found to be disrupted, and decreased tight junction protein expression was observed in palmitic acid-treated Sertoli cells. Palmitic acid entered the endoplasmic reticulum and induced endoplasmic reticulum stress, resulting in damage to Sertoli cell barriers.
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