MicroRNA signature in various cell types of mouse spermatogenesis: Evidence for stage‐specifically expressed miRNA‐221, ‐203 and ‐34b‐5p mediated spermatogenesis regulation

Smorag, Lukasz; Zheng, Ying; Nolte, Jessica; Zechner, Ulrich; Engel, Wolfgang; Pantakani, D. V. Krishna

doi:10.1111/boc.201200014

Cited by 84 publications

(76 citation statements)

References 54 publications

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“…ly, miR-34b-5p and miR-449a, which are members of the miR-34/449 family, have been reported to be preferentially expressed in the testis, especially in meiotic cells during spermatogenesis in mice (Smorag et al, 2012). Therefore, the down-regulation of miR-34b-5p and miR-449a might reflect the depletion of meiotic cells such as pachytene spermatocytes in EGME-treated monkeys.…”

Section: Discussionmentioning

confidence: 99%

“…The target miRNAs, miR-34b-5p and miR-449a in the testis, which were associated with spermatogenesis or EGME induced-testicular toxicity (Fukushima et al, 2011;Lizé et al, 2011;Smorag et al, 2012;Wu et al, 2014), were applied to RT-qPCR with 7900HT Fast Real Time PCR System (Applied Biosystems). The primers for miR-34b-5p and miR-449a (Assay IDs: #000427 and 001030) were designed based on each respective human sequence obtained from miRBase (http://microrna.sanger.…”

Section: Reverse Transcription-quantitative Real-time Pcr (Rt-qpcr) Amentioning

confidence: 99%

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MicroRNA profling in ethylene glycol monomethyl ether-induced monkey testicular toxicity model

et al. 2015

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-To establish and characterize ethylene glycol monomethyl ether (EGME)-induced testicular toxicity model in cynomolgus monkeys, EGME at 0 or 300 mg/kg was administered orally to sexually mature male cynomolgus monkeys (n = 3/group) for 4 consecutive days. Circulating and testicular micro-RNA (miRNA) profiles in this model were investigated using miRNA microarray or real-time quantitative reverse transcription-PCR methods. EGME at 300 mg/kg induced testicular toxicity in all the monkeys, which was characterized histopathologically by decreases in pachytene spermatocytes and round spermatids, without any severe changes in general conditions or clinical pathology. In microarray analysis, 16 down-regulated and 347 up-regulated miRNAs were detected in the testis, and 326 down-regulated but no up-regulated miRNAs were detected in plasma. Interestingly, miR-1228 and miR-2861 were identified as abundant miRNAs in plasma and the testis of control animals, associated presumably with apoptosis and cell differentiation, respectively, and were prominently increased in the testis of EGME-treated animals, reflecting the recovery from EGME-induced testicular damages via stimulating cell proliferation and differentiation of sperm. Furthermore, down-regulation of miR-34b-5p and miR-449a, which are enriched in meiotic cells like pachytene spermatocytes, was obvious in the testis, suggesting that these spermatogenic cells were damaged by the EGME treatment. In conclusion, EGME-induced testicular toxicity in cynomolgus monkeys was shown, and this model would be useful for investigating the mechanism of EGME-induced testicular toxicity and identifying testicular biomarkers. Additionally, testicular miR-34b-5p and miR-449a were suggested to be involved in damage of pachytene spermatocytes.

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Section: Discussionmentioning

confidence: 99%

Section: Reverse Transcription-quantitative Real-time Pcr (Rt-qpcr) Amentioning

confidence: 99%

MicroRNA profling in ethylene glycol monomethyl ether-induced monkey testicular toxicity model

et al. 2015

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“…Interestingly, miR-34c has also been shown to promote murine male germ cell apoptosis by targeting the transcription factor ATF1 in a p53-independent manner [122]. In mouse models, miR-34c and miR-34b were found to be highly expressed in post-mitotic male germ cells from primary spermatocytes up to round spermatids [121,123], and deletion of this locus along with miR-449 led to OAT and infertility [124]. Remarkably, miR-34c seems to extend its reproductive role into the zygote, as sperm-borne miR-34c has been shown to Patients with oligoospermia / oligoasthenozoospermia (80) and NOA (40) Spermatozoa and testicular tissues miR-429 was significantly increased, whereas miR-34b*, miR-34b, miR-34c-5p…”

Section: Spermatozoal Mirnas and Male Infertilitymentioning

confidence: 99%

The role of epigenetics in idiopathic male infertility

Güneş

Arslan

Hekim

et al. 2016

J Assist Reprod Genet

109

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Infertility is a complex disorder with multiple genetic and environmental causes. Although some specific mutations have been identified, other factors responsible for sperm defects remain largely unknown. Despite considerable efforts to identify the pathophysiology of the disease, we cannot explain the underlying mechanisms of approximately half of infertility cases. This study reviews current data on epigenetic regulation and idiopathic male infertility. Recent data have shown an association between epigenetic modifications and idiopathic infertility. In this regard, epigenetics has emerged as one of the promising research areas in understanding male infertility. Many studies have indicated that epigenetic modifications, including DNA methylation in imprinted and developmental genes, histone tail modifications and short non-coding RNAs in spermatozoa may have a role in idiopathic male infertility.

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“…For instance, it has been reported that all spermatogonia isolated from 8-day-old mice display detectable KIT mRNA, but 30-50% of these lack protein expression (Prabhu et al, 2006), presumably implying cell specific translational control mechanisms exerted by microRNA and/ or RNA-binding proteins, which are known to play fundamental roles in the regulation of spermatogenesis Messina et al, 2012). Very recently miRNA 221, which was previously known to target Kit mRNA in hematopoietic stem cells, has been shown to be specifically expressed in spermatogonial stem cells (Smorag et al, 2012), and evidence has been given that both KIT mRNA and KIT protein abundance are influenced by miRNA 221 and miRNA 222 function in spermatogonia (Yang et al, 2013). These results imply that, together with repression of Kit transcription exerted by PLZF, microRNAs actually contribute to post-transcriptional silencing of Kit expression in the spermatogonial stem cell pool.…”

Section: Transcription Factors Controlling Kit Expression In the Germmentioning

confidence: 99%

Transcriptional control of KIT gene expression during germ cell development

Rossi¹

2013

Int. J. Dev. Biol.

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The characterization of the mechanisms that regulate KIT expression in germ cells at different times of their development is important not only in the field of reproduction, but also for a better understanding of the biology of testicular germ cell tumors (TGCTs). Indeed this tyrosine kinase receptor, besides being essential for the survival and proliferation of primordial germ cells (PGCs) and for postnatal spermatogenesis and oogenesis, is also frequently overexpressed or constitutively active due to activating mutations in carcinoma in situ of the testis and in seminomas. In this review, I will summarize available data about the transcriptional mechanisms involved in the control of Kit expression in the germline. Variable mechanisms, involving different germ cell-specific transcription factors, are operating in the various developmental stages: SOX2 and SOHLH1/2 act as direct positive regulators in PGCs and in postnatal spermatogonia, respectively, whereas PLZF suppresses KIT expression in spermatogonial stem cells. DMRT1, acting through indirect mechanisms, suppresses KIT transcription in fetal gonocytes, while activating it in differentiating spermatogonia.

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MicroRNA signature in various cell types of mouse spermatogenesis: Evidence for stage‐specifically expressed miRNA‐221, ‐203 and ‐34b‐5p mediated spermatogenesis regulation

Cited by 84 publications

References 54 publications

MicroRNA profling in ethylene glycol monomethyl ether-induced monkey testicular toxicity model

MicroRNA profling in ethylene glycol monomethyl ether-induced monkey testicular toxicity model

The role of epigenetics in idiopathic male infertility

Transcriptional control of KIT gene expression during germ cell development

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