NCBI Summary:
microRNAs (miRNAs) are short (20-24 nt) non-coding RNAs that are involved in post-transcriptional regulation of gene expression in multicellular organisms by affecting both the stability and translation of mRNAs. miRNAs are transcribed by RNA polymerase II as part of capped and polyadenylated primary transcripts (pri-miRNAs) that can be either protein-coding or non-coding. The primary transcript is cleaved by the Drosha ribonuclease III enzyme to produce an approximately 70-nt stem-loop precursor miRNA (pre-miRNA), which is further cleaved by the cytoplasmic Dicer ribonuclease to generate the mature miRNA and antisense miRNA star (miRNA*) products. The mature miRNA is incorporated into a RNA-induced silencing complex (RISC), which recognizes target mRNAs through imperfect base pairing with the miRNA and most commonly results in translational inhibition or destabilization of the target mRNA. The RefSeq represents the predicted microRNA stem-loop. [provided by RefSeq, Sep 2009]
MiR-31 and miR-143 affect steroid hormone synthesis and inhibit cell apoptosis in bovine granulosa cells through FSHR. Zhang Z et al. (2018) The regulatory role of microRNAs (miRNAs) has been explored in ovarian cells, and the effects of miRNAs on gonadal development, apoptosis, ovulation, and steroid production have been reported. In this study, we analyzed the effects of follicle stimulating hormone (FSH) on miR-31 and miR-143 expression levels in bovine granulosa cells (GCs). Our results demonstrated that the FSH receptor (FSHR) is a common target gene of miR-31 and miR-143 in bovine GCs. We further analyzed the roles of miR-31 and miR-143 in bovine GCs by transfecting miR-31 and miR-143 mimics and inhibitors. The Western blot and RT-PCR results showed that miR-31 and miR-143 reduced the mRNA and protein expression levels of FSHR. Moreover, miR-31 overexpression decreased the secretion of progesterone (P4), and miR-143 overexpression decreased both the synthesis of P4 and the secretion of estrogen (E2). In contrast, miR-31 inhibition increased the secretion of progesterone (P4), and miR-143 inhibition increased both the synthesis of P4 and the secretion of E2. Finally, we analyzed the possible effects of miR-31 and miR-143 on bovine GC apoptosis. The results showed that transfection with miR-31 and miR-143 mimics promoted GC apoptosis and that miR-143 and miR-31 inhibition reduced the rate of apoptosis in bovine GCs. Taken together, our results indicate that miR-31 and miR-143 decrease steroid hormone synthesis and inhibit bovine GC apoptosis by targeting FSHR.////////////////// MiRNA-143 mediates the proliferative signaling pathway of FSH and regulates estradiol production. Zhang L et al. (2017) MicroRNAs (MiRNAs) play important regulatory roles in many cellular processes. MiR-143 is highly enriched in the mouse ovary, but its roles and underlying mechanisms are not well understood. In the current study, we show that miR-143 is located in granulosa cells of primary, secondary and antral follicles. To explore the specific functions of miR-143, we transfected miR-143 inhibitor into primary cultured granulosa cells to study the loss of function of miR-143 and the results showed that miR-143 silencing significantly increased estradiol production and steroidogenesis-related gene expression. Moreover, our in vivo and in vitro studies showed that follicular stimulating hormone (FSH) significantly decreased miR-143 expression. This function of miR-143 is accomplished by its binding to the 3'-UTR of KRAS mRNA. Furthermore, our results demonstrated that miR-143 acts as a negative regulating molecule mediating the signaling pathway of FSH and affecting estradiol production by targeting KRAS. MiR-143 also negatively acts in regulating granulosa cells proliferation and cell cycle-related genes expression. These findings indicate that miR-143 plays vital roles in FSH-induced estradiol production and granulosa cell proliferation, providing a novel mechanism that involves miRNA in regulating granulosa cell functions.////////////////// mir-143 is critical for the formation of primordial follicles in mice?. Zhang J et al. Although microRNAs (miRNAs) have been implicated in fine-tuning gene networks, the roles of mmu-mir-143 (miR-143) in mammalian ovary development have not been studied?in vitro. We investigated the expression and function of miR-143 in the mouse ovary during primordial follicle formation. Real-time polymerase chain reaction analysis showed that miR-143 expression increased during primordial follicle formation from 15.5 days post-coitus to 4 days post-partum. miR-143 was located in pregranulosa cells by?in situ?hybridization. To study the function of miR-143 in primordial follicle formation we established an electroporation transfection model?in vitro?that allowed miR-143 expression to be efficiently upregulated and inhibited in cultured ovaries. Further studies showed that miR-143 inhibited the formation of primordial follicles by suppressing pregranulosa cell proliferation and downregulating the expression of genes related to the cell cycle. These findings suggest that miR-143 is critical for the formation of primordial follicles and regulates ovarian development and function.
Expression regulated by
FSH
Comment
A network of miRNAs expressed in the ovary are regulated by FSH. Yao N et al. The process of folliculogenesis requires a tightly regulated series of gene expression that are a pre-requisite to the development of ovarian follicle. Among these genes, follicle-stimulating hormone (FSH) is notable for its dual role in development of follicles as well as proliferation and differentiation of granulosa cells. The post-transcriptional expression of these genes is under the control of microRNAs (miRNAs), a class of small, endogenous RNAs that negatively impact gene expression. This study was carried out to determine the role of several miRNAs including mir-143, let-7a, mir-125b, let-7b, let-7c, mir-21 in follicular development in the mouse. The expression of these RNAs was very low in primordial follicles but these became readily detectable in the granulosa cells of primary, secondary and antral follicles. We show that this expression of some miRNAs (mir-143, let-7a, mir-15b) is under negative control of FSH. Together, these findings suggest that FSH regulates folliculogenesis by a novel pathway of miRNAs.