Altered microRNA expression profiles of human spermatozoa in patients with different spermatogenic impairments

The role of epigenetics in idiopathic male infertility

“…Notably, increased expression patterns for these miRNAs were also observed in testicular tissues of patients with NOA, implicating the potential use of seminal miRNAs as noninvasive biomarkers for the diagnosis of male infertility. However, care must be taken to utilize these findings to make a differential diagnosis, as a previous study has also found similar fold inductions in miR-141 and miR-429 expression in spermatozoa from asthenozoospermic and oligoasthenozoospermic patients [105]. Moreover, miR-429 appears to be highly upregulated in spermatozoa from oligospermic males as well and to a lesser extent in testicular tissues of patients with NOA [108], consistent with the above finding [129].…”

“…A comprehensive miRNA microarray analysis of spermatozoa from nine asthenozoospermic and nine oligoasthenozoospermic men has revealed 50 upregulated, 27 downregulated miRNAs, and 42 upregulated, 44 downregulated miRNAs, respectively, when compared to normozoospermic men [105] (Table 2). The miRNAs that exhibited the highest fold changes were the ones that are downregulated, with most of them more than 10 times decreased in their expression levels.…”

“…The miRNAs that exhibited the highest fold changes were the ones that are downregulated, with most of them more than 10 times decreased in their expression levels. To name a few, miR-34b, miR-122, and miR-1973 were found to be downregulated in asthenozoospermic men, whereas miR-34b, miR-34b*, miR-34c-5p, miR-15b, miR-122, miR-449a, miR-1973, and miR-16 were downregulated in oligoasthenozoospermic men [105] (Table 2). Although bioinformatics analyses have predicted putative target genes of these miRNAs, detailed in vitro and in vivo studies linking most of them to their specific target genes within the context of male infertility are largely missing.…”

“…Given the crucial roles of estrogen receptor-α and -β in maintenance of male reproductive tract function, sperm metabolism and Sertoli cell proliferation, it would not be surprising if there exists a miRNA-based mechanism for downregulation of these two receptors in infertile men [118,119]. Using qRT-PCR, a validation study has tested the potential of a set of five differentially expressed miRNAs selected from the two aforementioned miRNA microarray analyses [105,107], to be used as biomarkers for the assessment of male infertility [108]. Spermatozoa from 80 subfertile (mostly oligospermic and oligoasthenospermic) men and testicular tissues from 40 men with non-obstructive azoospermia were analyzed along with their appropriate controls, and with the exception of miR-429, the expressions of all other four miRNAs (miR-34b*, miR-34b, miR-34c-5p, miR-122) were found to be decreased in both tested groups [108].…”

Mitochondrial DNA polymerase gamma gene polymorphism is not associated with male infertility

“…A large proportion of male infertility cases are due to systemic defects like reproductive organ impairment and defective sperm production with imbalance in levels of gonadal steroids most of which can be treated. Genetics contributes to infertility by influencing a variety of physiological processes including hormonal homeostasis, spermatogenesis, and sperm quality [1]. Therefore understanding of the genetic basis of reproductive failure is essential to appropriately counsel an infertile couple.…”