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Biomarkers in semen/urine from non-obstructive azoospermia patients to predict the presence of testicular spermatozoa and spermatogonia

ABSTRACT: Biomarkers in semen/urine from non-obstructive azoospermia patients to predict the presence of testicular spermatozoa and spermatogonia

PROVIDER: PRJNA931358 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23337500.fastq.gz	Fastqsanger.gz
	SRR23337501.fastq.gz	Fastqsanger.gz
	SRR23337502.fastq.gz	Fastqsanger.gz
	SRR23337503.fastq.gz	Fastqsanger.gz
	SRR23337504.fastq.gz	Fastqsanger.gz

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Biomarkers in semen/urine from non-obstructive azoospermia patients to predict the presence of testicular spermatozoa and spermatogonia

Project description:About half of testicular sperm extraction (TESE) procedures in men with non-obstructive azoospermia (NOA), including men with Klinefelter syndrome (KS), are unsuccessful. To avoid unnecessary invasive surgery, biomarkers for spermatozoa have been studied and identified. In addition, markers for spermatogonia in testis tissue have been researched. This study aimed to find biomarkers in semen and/or urine of NOA patients to predict the presence of spermatogonia in the testis. This would especially be interesting for young boys. Differentially expressed miRNAs were identified (1) between samples from patients with and those of patients without a positive TESE procedure as well as (2) between TESE negative patients with and those without spermatogonia. A total of ten up-regulated miRNAs (seven in seminal plasma and three in urine) were found in the TESE-negative/spermatogonia-positive group compared to the TESE-negative/spermatogonia-negative group. These miRNAs could become biomarkers for spermatogonia, however, more research is necessary.

2023-02-06 | GSE224511 | GEO

Comparative proteomics analysis of FFPE testicular tissue from men with obstructive and non-obstructive azoospermia

Project description:The project aimed to compare testicular proteomes from patients with obstructive and non-obstructive azoospermia in order to identify molecular signatures involved in spermatogenesis as well to identify candidate biomarkers for discriminating between different types of azoospermia. The samples used in this study were formalin fixed paraffin embedded (FFPE) testicular tissues obtained by biopsy from men with clinical diagnosis of azoospermia. Samples were grouped according to the histopathological report in 3 groups: 1) Spermatogenesis (obstructive azoospermia), 2) Hypospermatogenesis and 3) Sertoli cell only syndrome (SCO). Patients were aged 31–46 years with no differences among groups regarding age (Median age (Hypospermatogenesis) =35; Median age (SCO) =34 and Median age (Spermatogenesis) =39). Each group had 9 samples or 27 samples in total were used for the comparative proteomics analysis by label-free data-independent LC-MS/MS.

2022-07-31 | PXD032722 | Pride

Whole Exome Sequencing of two non-obstructive azoospermia patients

Project description:We collected blood samples of two non-obstructive azoospermia patients, and performed whole exome sequencing to explore the causal mutations for male infertility.

2021-06-22 | E-MTAB-9287 | biostudies-arrayexpress

In situ transcriptomic analysis of spermatocytes in non-obstructive azoospermia reveals senescence-like states in arrested spermatocytes

Project description:To investigate in situ transcriptome of spermatocytes in non-obstructive azoospermia , we microdissected spermatocytes in formalin-fixed paraffin-embedded testicular biopsy tissue from two types of non-obstructive azoospermia and obstructive azoospermia as a control, and then constructed cDNA libraries based on Smart-3SEQ method.

2023-08-02 | GSE238078 | GEO

Transcription profiling of testis biopsies to investigate testis developmental gene expression in cryptorchid boys at risk of azoospermia

Project description:Despite timely and successful surgery, 32% of patients with bilateral and 10% with unilateral cryptorchidism will develop azoospermia. Cryptorchid boys at risk of azoospermia display a typical testicular histology of impaired mini-puberty at the time of the orchidopexy. During mini-puberty increased gonadotropin and testosterone secretion stimulate transformation of gonocytes into Ad spermatogonia. In azoospermia risk group this transformation is to a great extent impaired. This study aimed to analyze data on whole genome expression signatures of undescended testes at risk of developing azoospermia. Twenty-three testicular biopsies from 22 boys were analyzed (19 testes from 18 boys with cryptorchidism) and 4 contralateral descended testes from patients with testicular agenesis. Expression profiling identified 483 genes not or under-expressed in the azoospermia risk group compared with the control and LAZR groups. Annotated loci were associated with spermatogenesis. Other significant genes were cellular defense response genes and hormone controlled loci involved in spermatogenesis. Some genes transcribed in normal adult meiotic and post-meiotic germ cells are activated in healthy juvenile Ad spermatogonia. Thus, molecular events initiating the testicular expression program at the onset of puberty and maintaining it during adulthood occur very early in prepubertal testes. This molecular event is to a great extent impaired in HAZR group lacking Ad spermatogonia (stem cells for spermatozoa) indicating impaired mini puberty.

2010-11-23 | E-GEOD-25518 | biostudies-arrayexpress

Micro RNA in Semen/Urine from Non-Obstructive Azoospermia Patients as Biomarkers to Predict the Presence of Testicular Spermatozoa and Spermatogonia.

Project description:About half of testicular sperm extraction (TESE) procedures in men with non-obstructive azoospermia (NOA), including men with Klinefelter syndrome (KS), are unsuccessful. To avoid unnecessary invasive surgery, biomarkers for spermatozoa were studied. In addition, markers for spermatogonia in testis tissue were explored. This study aimed to find biomarkers in the semen and/or urine of NOA patients to predict the presence of spermatogonia in the testis. Differentially expressed miRNAs were identified (1) between samples from patients with and without a positive TESE procedure as well as (2) between TESE-negative patients with and without spermatogonia. A total of thirteen upregulated miRNAs (ten in seminal plasma and three in urine) were found in the TESE-negative/spermatogonia-positive group compared to the TESE-negative/spermatogonia-negative group. These miRNAs could be potential biomarkers for spermatogonia; however, more research is necessary to validate their predictive power.

| S-EPMC10051987 | biostudies-literature

Whole Exome Sequencing of two non-obstructive azoospermia patients

Project description:Whole Exome Sequencing of two non-obstructive azoospermia patients

| PRJEB39182 | ENA

Altered mRNA profile in testis of patients with“secondary idiopathic non-obstructive azoospermia”

Project description:Background: Non-obstructive azoospermia (NOA) is the most severe form of male infertility. Currently known causative factors, including congenital and several acquired causes can only account for approximately 30% of NOA cases. Causes for most patients with NOA remains unclear, which were known as idiopathic NOA (iNOA). However, whether iNOA is congenital defects or acquired abnormalities is a confusing problem due to the delayed diagnosis of this frustrating situation until childbearing age. Materials and Methods: In this study, several patients who were diagnosed as iNOA at this stage, but with a history of natural conceptions with female before were enrolled and defined as “secondary idiopathic NOA”. As little was known about these cases, we performed the mRNA expression profiling by Next-generation sequencing (NGS) in this three patients and other three patients with obstructive azoospermia (OA) as controls. Results: A series of mRNAs were found to be altered in testicular tissues between “secondary idiopathic NOA” and controls, including 6028 downregulated and 3402 upregulated mRNAs. GO analysis and KEGG analysis revealed a range of GO and KEGG terms, such as cellular process involved in reproduction, protein digestion and absorption, etc. Conclusion: Overall, this study introduces a novel classification called “secondary idiopathic NOA” in iNOA. We provide a global view of the altered mRNAs involved in spermatogenetic failure in these cases.

2022-06-01 | GSE190752 | GEO

Whole Transcriptome analysis to identify non-coding RNA regulators and hub genes in Sperm of non-obstructive azoospermia by microarray

Project description:Our study utilizes whole transcriptome analysis via microarray technology to uncover non-coding RNA regulators and hub genes within sperm samples afflicted by non-obstructive azoospermia. This comprehensive approach offers insight into the intricate molecular landscape underlying this condition, shedding light on potential regulatory mechanisms and key genetic players implicated in its pathogenesis.

2024-05-31 | GSE268452 | GEO

Proteomic analysis of rabbit fresh and cryopreserved semen (spermatozoa)

Project description:Cryoinjury and protein changes are a consequence of cryopreservation and may have a negative impact on sperm quality regarding motility, viability and fertilizing ability. However, potential proteomic changes in rabbit semen throughout the cryopreservation process have never been investigated previously. The aim of the present study was to compare the whole proteome of fresh and cryopreserved rabbit spermatozoa. Comparative analysis and identification of proteins were performed using 2-dimensional difference in-gel electrophoresis (2D-DIGE) coupled with matrix-assisted laser desorption/ionization mass (MALDI TOF/TOF) spectrometry. We found that 108 proteins differed in abundance in spermatozoa between fresh and frozen semen. Most of these proteins was involved in pathways related to energy metabolism and protein quality control under stress conditions, reproductive processes and mechanisms of cell death/survival regulation, resulting in a significant decrease of motility and viability of post-thawing rabbit sperm and its potential fertilizing ability.

2022-10-14 | PXD034832 | Pride

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