Regulation of GVBD in mouse oocytes by miR-125a-3p and Fyn kinase through modulation of actin filaments

Grossman, Hadas; Har-Paz, Efrat; Gindi, Natalie; Levi, Mattan; Miller, Irit; Nevo, Nava; Galiani, Dalia; Dekel, Nava; Shalgi, Ruth

doi:10.1038/s41598-017-02071-x

Cited by 12 publications

(10 citation statements)

References 74 publications

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“…In a previous study we found that the decrease in the expression of oocyte miR-125a-3p, caused by hCG, was required for resumption of the first meiotic division (Grossman et al 2017). Surprisingly, unlike in oocytes exposed to hCG in vivo, we observed an increase in the expression of miR-125a-3p within oocytes derived from CBX-treated follicles, instead of the expected decrease.…”

Section: Discussioncontrasting

confidence: 70%

“…The decreased ability of miRNAs to inhibit the expression of the luciferase reporter suggests that distinct miRNAs might be subjected to different regulatory mechanisms to enable a time-restricted activity of miRNAs. The regulation, by hCG, of miR-125a-3p expression in oocytes suggests that it is one of the miRNAs that play a role in fully grown GV oocytes, a suggestion supported by our recent finding that miR-125a-3p participates in maintaining the first meiotic arrest by modulating the actin cytoskeleton (Grossman et al 2017).…”

Section: Discussionmentioning

confidence: 58%

“…Our previous studies, both in HEK-293T cells (Ninio-Many et al 2013) and in rodent GCs (Grossman et al 2015), have established miR-125a-3p as a posttranscription regulator of Fyn. The expression of miR-125a-3p decreases in mouse oocytes during maturation; overexpression of miR-125a-3p inhibits resumption of the first meiotic division, through modulation of Fyn expression (Grossman et al 2017). The preovulatory expression of miR-125a-3p in mural GCs was downregulated by human-chorionic gonadotropin (hCG; an LH analog), enabling the increase in the expression of Fyn and promoting the migratory ability of the cells; both required for proper ovulation (Grossman et al 2015).…”

Section: Introductionmentioning

confidence: 99%

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Pre-ovulatory intercellular regulation of miR-125a-3p within mouse ovarian follicles

et al. 2020

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miR-125a-3p, a post-transcription regulator of Fyn kinase, is expressed in mouse pre-ovulatory follicles; its expression within the follicle decreases toward ovulation. Our aim was to follow the synthesis of miR-125a-3p and regulation of its expression in all follicular compartments, focusing on intercellular communication. Mural granulosa cells (GCs) or cumulus cells (CCs) were transfected with either scrambled-miR (negative control) or miR-125a-3p mimic. Freshly isolated GCs or CCs were incubated overnight in culture media conditioned by transfected cells. To examine a possible role of gap junctions in the regulation of miR-125a-3p, we incubated large antral follicles in the presence of carbenoxolone, a gap-junction inhibitor, and triggered them to mature with hGC. Levels of miR-125a family members in GCs, CCs, oocytes, and culture media were measured by qPCR. We showed that miR-125a-3p is synthesized by all follicular components, but is regulated within the follicle as a whole. It is secreted by mural-GCs and taken up by CCs, where it remains functional, and vice versa, mural-GCs can take up miR-125a-3p secreted by CCs. miR-125a-3p is transcribed and accumulated in oocytes throughout oogenesis. Transcriptionally quiescent GV oocytes utilize their accompanying follicular cells to monitor the level of miR-125a-3p within them, as indicated in an ex vivo follicle culture. Our study reveals that miR-125a-3p expression is modulated by a network of intercellular communications within pre-ovulatory follicles, thus enabling a coordinated decrease of miR-125a-3p toward ovulation.

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Section: Discussioncontrasting

confidence: 70%

Section: Discussionmentioning

confidence: 58%

Section: Introductionmentioning

confidence: 99%

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Pre-ovulatory intercellular regulation of miR-125a-3p within mouse ovarian follicles

et al. 2020

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“…Interestingly, in vitro functional study of miR-130b showed the involvement of this miRNA in oocyte maturation by regulating the SMAD5 and MSK1genes [44]. Similarly, other studies have shown the role of miR-318 [45], miR-202 [46] and let-7, miR-278 [47], miR-378 [48] and miR-125a-3p [49] during oogenesis.…”

Section: The Role Of Cellular Mirnas In Follicular Development and Oomentioning

confidence: 82%

The Role of MicroRNAs in Mammalian Fertility: From Gametogenesis to Embryo Implantation

Salilew‐Wondim

Gebremedhn

Hoelker

et al. 2020

IJMS

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The genetic codes inscribed during two key developmental processes, namely gametogenesis and embryogenesis, are believed to determine subsequent development and survival of adult life. Once the embryo is formed, its further development mainly depends on its intrinsic characteristics, maternal environment (the endometrial receptivity), and the embryo–maternal interactions established during each phase of development. These developmental processes are under strict genetic regulation that could be manifested temporally and spatially depending on the physiological and developmental status of the cell. MicroRNAs (miRNAs), one of the small non-coding classes of RNAs, approximately 19–22 nucleotides in length, are one of the candidates for post-transcriptional developmental regulators. These tiny non-coding RNAs are expressed in ovarian tissue, granulosa cells, testis, oocytes, follicular fluid, and embryos and are implicated in diverse biological processes such as cell-to-cell communication. Moreover, accumulated evidences have also highlighted that miRNAs can be released into the extracellular environment through different mechanisms facilitating intercellular communication. Therefore, understanding miRNAs mediated regulatory mechanisms during gametogenesis and embryogenesis provides further insights about the molecular mechanisms underlying oocyte/sperm formation, early embryo development, and implantation. Thus, this review highlights the role of miRNAs in mammalian gametogenesis and embryogenesis and summarizes recent findings about miRNA-mediated post-transcriptional regulatory mechanisms occurring during early mammalian development.

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“…We assessed mRNA and miRNA expression in oocytes and blood of F0 females, and in the AMY and PFC of F0 females and their neonate and adult F1 and F2 offspring. Dissections, RNA and miRNA extraction, cDNA preparation, and quantitative real-time PCR (qRT-PCR) were performed as described previously 29 , 48 , 49 (see Table S 3 for primer list). Fold-change values were calculated using the ddCt method 50 relative to the housekeeping gene hypoxanthine phosphoribosyl transferase (HPRT; mRNA; brain), 18s (mRNA; oocytes), or U6-snRNA/RNU6 (miRNA), which were found to be expressed in similar levels across groups and tissue types.…”

Section: Methodsmentioning

confidence: 99%

Pre-reproductive stress in adolescent female rats alters oocyte microRNA expression and offspring phenotypes: pharmacological interventions and putative mechanisms

2021

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Pre-reproductive stress (PRS) to adolescent female rats alters anxiogenic behavior in first (F1)- and second-generation (F2) offspring and increases mRNA expression of corticotropin-releasing factor receptor type 1 (Crhr1) in oocytes and in neonate offspring brain. Here, we ask whether the expression of Crhr1 and Crhr1-targeting microRNA is altered in brain, blood, and oocytes of exposed females and in the brain of their neonate and adult F1 and F2 offspring. In addition, we inquire whether maternal post-stress drug treatment reverses PRS-induced abnormalities in offspring. We find that PRS induces a selective increase in Crhr1-targeting mir-34a and mir-34c in blood and oocytes, while non-Crhr1 microRNA molecules remain unaltered. PRS induces similar microRNA changes in prefrontal cortex of F1 and F2 neonates. In adult animals, cortical Crhr1, but not mir-34, expression is affected by both maternal and direct stress exposure. Post-PRS fluoxetine (FLX) treatment increases pup mortality, and both FLX and the Crhr1 antagonist NBI 27914 reverse some of the effects of PRS and also have independent effects on F1 behavior and gene expression. PRS also alters behavior as well as gene and miRNA expression patterns in paternally derived F2 offspring, producing effects that are different from those previously found in maternally derived F2 offspring. These findings extend current knowledge on inter- and trans-generational transfer of stress effects, point to microRNA changes in stress-exposed oocytes as a potential mechanism, and highlight the consequences of post-stress pharmacological interventions in adolescence.

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Regulation of GVBD in mouse oocytes by miR-125a-3p and Fyn kinase through modulation of actin filaments

Cited by 12 publications

References 74 publications

Pre-ovulatory intercellular regulation of miR-125a-3p within mouse ovarian follicles

Pre-ovulatory intercellular regulation of miR-125a-3p within mouse ovarian follicles

The Role of MicroRNAs in Mammalian Fertility: From Gametogenesis to Embryo Implantation

Pre-reproductive stress in adolescent female rats alters oocyte microRNA expression and offspring phenotypes: pharmacological interventions and putative mechanisms

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