Cross-platform gene expression signature of human spermatogenic failure reveals inflammatory-like response

Spiess, Andrej‐Nikolai; Feig, Caroline; Schulze, Wolfgang; Chalmel, Frédéric; Cappallo-Obermann, Heike; Primig, Michael; Kirchhoff, Christiane

doi:10.1093/humrep/dem292

Cited by 75 publications

(61 citation statements)

References 51 publications

(67 reference statements)

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“…As shown by Spiess et al, 10 the microarray-based analysis of mRNA levels in testicular biopsies from fertile men and from men with different types of spermatogenic failure is highly reliable: in 19 of 20 genes tested, the expression patterns could be confirmed by quantitative RT-PCR. 10 For validation of the gene-expression data described here, we used a second, independent dataset of human spermatogenesis.…”

Section: Discussionmentioning

confidence: 84%

“…10 For validation of the gene-expression data described here, we used a second, independent dataset of human spermatogenesis. 11 Except for EZH2 and MBD1, concordant expression profiles were found.…”

Section: Discussionmentioning

confidence: 99%

“…Owing to the limited availability of normal human testis samples and technical problems associated with RNA in situ hybridization of this material, we have mined gene-expression data of testicular biopsies from men with different types of spermatogenic failure (complete tubular atrophy, Sertoli-cell only syndrome, arrest before meiosis, arrest at meiosis, arrest at round spermatids, and uniform hypospermatogenesis) and with full spermatogenesis. 10 We show that these data can be used to infer gene-expression levels in spermatogonia, spermatocytes and round spermatids.…”

Section: Introductionmentioning

confidence: 94%

“…The expression data of spermatogenesis genes, genes encoding DNA and histone-binding and -modifying proteins, as well as the SNURF -SNRPN upstream transcripts were extracted from the dataset published by Spiess et al 10 To corroborate the findings, which were obtained with Affymetrix GeneChip microarrays (Affymetrix, Santa Clara, CA, USA), we included expression data acquired with a completely different platform based on single-oligonucleotide probes (Codelink system, Applied Microarray Inc., Tempe, AZ, USA) in the analysis. 11 This was done by building an intersection of the two platforms using HUGO gene abbreviations.…”

Section: Expression Profilesmentioning

confidence: 99%

“…To address these questions we have mined gene-expression data of testicular biopsies from men with different types of spermatogenic failure as determined with Affymetrix GeneChips. 10 The arrest types used in this study differ essentially in their germ-cell composition so that data can be extracted by filtering genes that pertain to those germ-cell types that appear from a higher impaired pathology to a lower one. In detail, this would be the following (using the abbreviations defined in the legend to To determine whether these data can be used to determine the upregulation of genes at specific stages of spermatogenesis, we examined several spermatogenesis genes.…”

Section: Expression Profilesmentioning

confidence: 99%

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Expression of SNURF–SNRPN upstream transcripts and epigenetic regulatory genes during human spermatogenesis

et al. 2009

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The imprinted domain in human 15q11-q13 is controlled by a bipartite imprinting centre (IC), which overlaps the 5 0 part of the paternally expressed SNURF -SNRPN gene. We have recently described two novel genes upstream of SNURF-SNRPN (PWRN1 and PWRN2), which are biallelically expressed in the testis. We have now found that PWRN1 represents an alternative 5 0 part of SNURF -SNRPN, and that its expression in the brain is imprinted. To determine when the locus is activated during spermatogenesis and which factors are involved in this process, we have mined gene-expression data of testicular biopsies from men with different types of spermatogenic failure. Whereas PWRN1-SNURF-SNRPN and PWRN2 are expressed in post-meiotic germ cells only, a hitherto undetected SNURF-SNRPN upstream transcript is expressed already at meiosis. Several epigenetic factors (eg, MBD1 and MBD2 isoforms, MBD3L1, SUVH39H2, BRDT, and EZH2) are upregulated at specific stages of spermatogenesis, suggesting that they play an important role in the epigenetic reprogramming during spermatogenesis.

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Section: Discussionmentioning

confidence: 84%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 94%

Section: Expression Profilesmentioning

confidence: 99%

Section: Expression Profilesmentioning

confidence: 99%

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Expression of SNURF–SNRPN upstream transcripts and epigenetic regulatory genes during human spermatogenesis

et al. 2009

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Cytokines and chemokines in testicular inflammation: A brief review

Guazzone

Jacobo

Theas

et al. 2009

Microscopy Res & Technique

181

131

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A wide spectrum of data in the literature shows the relevance of cytokines as paracrine regulators of spermatogenesis and steroidogenesis in the normal testis. In this brief review, we highlight the relevance of cytokines in the testis during inflammation. This phenomenon involves complex and multiple interactions among immune and germ cells generally resulting in the alteration of spermatogenesis. The complexity of these cell interactions is multiplied because Sertoli and Leydig cells are also producers of pro- and anti-inflammatory cytokines and chemokines. Also, cytokines are pleiotropic and they exert opposite and/or redundant effects in different conditions. However, in spite of this bidirectional immunoregulatory function of cytokines, the mass of the data, reported from experiments of acute testicular inflammation, shows upregulation of interleukin (IL)-1beta, IL-1alpha, IL-6, and tumor necrosis factor alpha (TNF-alpha), which induce adverse effects on germ cells. In autoimmune orchitis, a chronic testicular inflammation, chemokines such as CCL2, CCL3, and CCL4 induce attraction and extravasation of immune cells within the testicular interstitium. These cells alter the normal immunosuppressor microenvironment principally through the secretion of proinflammatory cytokines, interferon-gamma initially, and IL-6 and TNF-alpha thereafter. Germ cells expressing TNFR1, IL-6R, and Fas increase in number and undergo apoptosis, through the TNF-alpha/TNFR1, IL-6/IL-6R, and Fas/Fas L systems. The knowledge of immune-germ and somatic testicular cell interactions will contribute to the understanding of the mechanisms by which chronic inflammatory conditions of the testis can disrupt the process of spermatogenesis.

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New Approaches to Diagnosing Male Infertility, Part I: Microarray Analysis of Testicular Biopsy Specimens from Men with Intact and Impaired Spermatogenesis

Spiess

Schulze

2012

Atlas on the Human Testis

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Cross-platform gene expression signature of human spermatogenic failure reveals inflammatory-like response

Abstract: A gene expression signature of human spermatogenic failure was revealed which comprised well-studied examples of inflammation-related genes also increased in other pathologies, including autoimmune diseases.

Cited by 75 publications

References 51 publications

Expression of SNURF–SNRPN upstream transcripts and epigenetic regulatory genes during human spermatogenesis

Expression of SNURF–SNRPN upstream transcripts and epigenetic regulatory genes during human spermatogenesis

Cytokines and chemokines in testicular inflammation: A brief review

New Approaches to Diagnosing Male Infertility, Part I: Microarray Analysis of Testicular Biopsy Specimens from Men with Intact and Impaired Spermatogenesis

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