<i>MiR‐98</i> is involved in rat embryo implantation by targeting <i>Bcl‐xl</i>

Xia, Hong-Fei; Jin, Xiaohua; Cao, Zongfu; Shen, Tian; Ma, Xu

doi:10.1016/j.febslet.2013.12.026

Cited by 31 publications

(19 citation statements)

References 21 publications

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“…Translated to the in vivo situation, we predict that such an effect might delay implantation to the point where corpus luteum rescue would not occur, leading to a failed pregnancy. Data from the rat similarly point to a role for miRs in regulating endometrial cell function in the implantation window (Xia et al, 2014a;Xia et al, 2014b). Such a prediction in human must be tempered by the limitations of the in vitro model, which includes the use of mouse embryos and cells from a welldifferentiated adenocarcinoma.…”

Section: Discussionmentioning

confidence: 99%

miR-145 suppresses embryo-epithelial juxtacrine communication at implantation by modulating maternal IGF1R

Kang

Lees

Matthews

et al. 2015

Journal of Cell Science

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Successful implantation requires the synchronization of viable embryonic development with endometrial receptivity. The mechanisms allowing for the initiation of crosstalk between the embryo and the endometrium remain elusive; however, recent studies have revealed that there are alterations in endometrial microRNAs (miRs) in women suffering repeated implantation failure and that one of the altered miRs is miR-145. We assessed the role of miR-145 and its target IGF1R, in early implantation. miR-145 overexpression and IGF1R knockdown were achieved in Ishikawa endometrial cells. Quantitative PCR, western blotting and 39UTR luciferase reporter assays confirmed that IGF1R is a direct target of miR-145 in the endometrium. Attachment of mouse embryos or IGF1-coated beads to endometrial epithelial cells was used to study the effects of altered miR-145 and/or IGF1R expression on early implantation events. miR-145 overexpression or specific reduction of IGF1R impaired attachment in both cases. An IGF1R target protector prevented the miR-145-mediated reduction in IGF1R and reversed the effect of miR-145 overexpression on attachment. The data demonstrate that miR-145 influences embryo attachment by reducing the level of IGF1R in endometrium.

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Section: Discussionmentioning

confidence: 99%

miR-145 suppresses embryo-epithelial juxtacrine communication at implantation by modulating maternal IGF1R

Kang

Lees

Matthews

et al. 2015

Journal of Cell Science

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“…MiR-98 expression is up-regulated in kidney in response to diabetes complications in mouse in and down-regulated in muscle in type 2 diabetes with insulin resistance in human910. Also, miR-98 is found to participate in embryo implantation during early pregnancy11. Although miR-98 is involved in T2DM and early pregnancy in the available literature91011, the relationship between miR-98 and GDM remains unknown, and roles of miR-98 in GDM are still unclear.…”

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confidence: 99%

“…Also, miR-98 is found to participate in embryo implantation during early pregnancy11. Although miR-98 is involved in T2DM and early pregnancy in the available literature91011, the relationship between miR-98 and GDM remains unknown, and roles of miR-98 in GDM are still unclear.…”

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confidence: 99%

Up-regulation of miR-98 and unraveling regulatory mechanisms in gestational diabetes mellitus

Cao

Lü

et al. 2016

Sci Rep

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MiR-98 expression was up-regulated in kidney in response to early diabetic nephropathy in mouse and down-regulated in muscle in type 2 diabetes in human. However, the expression prolife and functional role of miR-98 in human gestational diabetes mellitus (GDM) remained unclear. Here, we investigated its expression and function in placental tissues from GDM patients and the possible molecular mechanisms. The results showed that miR-98 was up-regulated in placentas from GDM patients compared with normal placentas. MiR-98 over-expression increased global DNA methylational level and miR-98 knockdown reduced global DNA methylational level. Further investigation revealed that miR-98 could inhibit Mecp2 expression by binding the 3′-untranslated region (UTR) of methyl CpG binding protein 2 (Mecp2), and then led to the expression dysregulation of canonical transient receptor potential 3 (Trpc3), a glucose uptake related gene. More importantly, in vivo analysis found that the expression level of Mecp2 and Trpc3 in placental tissues from GDM patients, relative to the increase of miR-98, was diminished, especially for GDM patients over the age of 35 years. Collectively, up-regulation of miR-98 in the placental tissues of human GDM is linked to the global DNA methylation via targeting Mecp2, which may imply a novel regulatory mechanism in GDM.

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“…Among the 6 apoptosis-related miRNAs we selected for RT-qPCR analysis, whereas miR-21 was antiapoptotic [33,34], miR-29b [35,36], miR-15a and miR-16 [37,38], miR-128 [39,40] and miR-98 [41,42; the present results] were pro-apoptotic. However, all these 6 apoptosis-related miRNAs significantly increased their expression from 18 to 24 h post hCG.…”

Section: Discussionmentioning

confidence: 88%

“…In addition, this study shows that miR-98 facilitated oocyte aging by increasing Ca 2+ release through activating caspase-3. There are also reports that miR-98 promoted apoptosis by down regulating Bcl-xl [42], HMGA2 [41] or cyclin D2 [69]. However, other studies found that miR-98 suppressed apoptosis by down regulating Fas expression [70] or by directly targeting caspase-3 [71,72].…”

Section: Discussionmentioning

confidence: 99%

Expression profiles and function analysis of microRNAs in postovulatory aging mouse oocytes

Wang

Zhang

Zhu

et al. 2017

Aging

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In this study, microRNA (miRNA) profiles in postovulatory aging mouse oocytes were analyzed by microarray screening and RT-qPCR. Hierarchical cluster analysis on the microarray data and KEGG pathway enrichment analysis on the mRNAs targeted by differentially expressed (DE) miRNAs between two adjacent egg-ages suggest that while only a mild alteration in miRNA expression occurred from 13 to 18 h, a great change took place from 18 to 24 h post hCG injection. Theoretical exploration on functions of the predicted target genes suggest that KEGG pathways enriched by 13-18 h DE miRNAs are correlated with early events of oocyte aging while pathways most enriched by 18-24 h or 24-30 h DE miRNAs are correlated with the late symptoms of aged oocytes. Experimental verification on functions of the key proteins predicted by the KEGG analysis and injection of miR-98 mimics or inhibitors further confirmed that miRNAs played stimulatory/inhibitory roles in postovulatory oocyte aging. In conclusion, marked changes in miRNA expression are associated with significant alterations in function and morphology of postovulatory aging oocytes.

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MiR‐98 is involved in rat embryo implantation by targeting Bcl‐xl

Cited by 31 publications

References 21 publications

miR-145 suppresses embryo-epithelial juxtacrine communication at implantation by modulating maternal IGF1R

miR-145 suppresses embryo-epithelial juxtacrine communication at implantation by modulating maternal IGF1R

Up-regulation of miR-98 and unraveling regulatory mechanisms in gestational diabetes mellitus

Expression profiles and function analysis of microRNAs in postovulatory aging mouse oocytes

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