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Asthenozoospermia (AZS), which characterised by reduced forward sperm motility, is a common cause of male infertility. Recently, mitochondrial dysfunction reported in AZS men came to attention for finding the molecular aetiology of AZS. Mitochondria-related microRNAs (miRNAs) are the most important regulators of mitochondrial function through post-transcriptionally modulation of gene expression. Therefore, this study aims to evaluate the expression of four recently reported mitochondrial-related miRNAs (miR-4485-3p/4484/4461 and 4463) in the sperm sample of asthenozoospermic men. RNA was extracted from spermatozoa of 74 volunteers (39 patients with idiopathic AZS and 35 controls with normal fertility), and relative gene expression analysis was performed by quantitative PCR. We used SNORD48 as a normaliser gene, and quantification was calculated by 2 -ΔΔCt method. The expression of miR-4484 and miR-4461 was not detected in the spermatozoa of cases and controls. However, miR-4485-3p (p = .006) was significantly downregulated in the AZS men compared with the controls, but the miR-4463 expression was not significantly different between the two groups (p = .5). Bioinformatic analysis identified three target genes for miR-4485-3p (DNAH1, KIT and PARK7) that are related to male infertility. In conclusion, the downregulation of miR-4485-3p was associated with idiopathic AZS, which could be a molecular link between mitochondrial dysfunction and AZS., (© 2020 Blackwell Verlag GmbH.)

Asthenozoospermia (AZS) which is characterised by decreased sperm motility is one of the main causes of male infertility. Recent studies demonstrated altered microRNAs (miRNAs) in total semen, seminal plasma and spermatozoa of asthenozoospermic men. In line with these studies, it was aimed to evaluate the miRNA expression profile in spermatozoa of unexplained asthenozoospermic men. Thirty-nine cases with idiopathic AZS and 35 fertile and healthy men as control were included. After total RNA extraction from spermatozoa, high-throughput sequencing technology was employed to display miRNA profiles in spermatozoa samples pooled from AZS cases and healthy controls. Relative quantification by real-time PCR was performed to validate RNA-seq results. SNORD48 was used as normaliser gene, and fold change was calculated by 2 -ΔΔCt method. Profiling results showed that 18 altered miRNAs in AZS men in comparison to controls. Subsequently, seven miRNAs were selected to validate by RT-PCR that showed MiR-888-3p significantly overexpressed in AZS cases (p = 0.014) in comparison with controls. It seems upregulation of miR-888-3p was associated with idiopathic AZS. This finding paves the way to the future investigation on the actual molecular role of miR-888-3p in aetiology of AZS., (© 2019 Blackwell Verlag GmbH.)

Infertility is a worldwide problem affecting about 15% of couples trying to conceive. Asthenozoospermia (AZS) is one of the major causes of male infertility, diagnosed by reduced sperm motility, and has no effective therapeutic treatment. To date, a few genes have been found to be associated with AZS in humans and mice, but in most of cases its molecular aetiology remains unknown. Genetic causes of AZS may include chromosomal abnormalities, specific mutations of nuclear and mitochondrial genes. However recently, epigenetic factors, altered microRNAs expression signature, and proteomics have shed light on the pathophysiological basis of AZS. This review article summarises the reported genetic causes of AZS. [ABSTRACT FROM AUTHOR]

Background: The purpose of this study was to analyze the expression level of CRISP2, CATSPER1, PATE1 and SEMG1 genes in the sperm of men with asthenozoospermia (AZS). AZS is a cause of infertility in men in which the motility of the sperm is reduced. So far, a few genes have been associated with AZS; however, in most of the cases, its molecular etiology is unclear. Methods: A total of 35 subjects with idiopathic AZS and 35 fertile and healthy men as control were included. In study after total RNA extraction and cDNA synthesis, relative quantification was performed. B2M was used as the normalizer gene and fold change was calculated by 2-ΔΔCt method. Mann-Whitney test was used to compare the expression levels between the case and control groups with significance level of p<0.05. Results: Our results showed that CRISP2 (p=0.03) and SEMG1 (p=0.03) were significantly down- and up-regulated in AZS men respectively compared to the controls. But CATSPER1 and PATE1 did not show significant changes. Conclusion: Down-regulation of CRISP2 and up-regulation of SEMG1 were associated with AZS, which could be suggested as the potential candidate genes for the development of a diagnostic marker or potentially for more studies for treatment of AZS. [ABSTRACT FROM AUTHOR]