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MicroRNA-200c impairs uterine receptivity formation by targeting FUT4 and ?1,3-fucosylation.

ABSTRACT: Successful embryo implantation requires the establishment of a receptive endometrium. Poor endometrial receptivity has generally been considered as a major cause of infertility. Protein glycosylation is associated with many physiological and pathological processes. The fucosylation is catalyzed by the specific fucosyltransferases. Fucosyltransferase IV (FUT4) is the key enzyme for the biosynthesis of ?1,3-fucosylated glycans carried by glycoproteins, and the previous studies showed FUT4 expression changed dynamically during perimplantation. MicroRNAs (miRNAs) are known to regulate specific gene expression. However, the relationship between specific miRNA and FUT4, as well as the role of miRNA/FUT4 in the establishment of uterine receptivity remains elusive. In the current study, we reported that the levels of miR-200 family members were significantly increased in serum from infertility and abortion patients relative to healthy non-pregnancy and early-pregnancy women. Among these, miR-200c was the most sensitive diagnostic criterion for infertility by receiver operating characteristic curve analysis. FUT4 was lower in the serum from infertility and abortion patients compared with the healthy non-pregnancy and early-pregnancy women. Using endometrial cell lines and a mouse model, we demonstrated that miR-200c targeted and inhibited FUT4 expression, leading to the dysfunction of uterine receptivity. Our results also revealed that miR-200c decreased ?1.3-fucosylation on glycoprotein CD44, which further inactivated Wnt/?-catenin signaling pathway. Taken together, miR-200c hampers uterine receptivity formation by targeting FUT4 and ?1.3-fucosylation on CD44. miR-200c and FUT4 may be applied together as the potential markers for endometrial receptivity, and useful diagnostic and therapeutic targets for infertility.

SUBMITTER: Zheng Q

PROVIDER: S-EPMC5686352 | biostudies-literature | 2017 Dec

REPOSITORIES: biostudies-literature

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MicroRNA-200c impairs uterine receptivity formation by targeting FUT4 and α1,3-fucosylation.

Zheng Qin Q Zhang Dandan D Yang Y U YU Cui Xinyuan X Sun Jiaqi J Liang Caixia C Qin Huamin H Yang Xuesong X Liu Shuai S Yan Qiu Q

Cell death and differentiation 20170915 12

Successful embryo implantation requires the establishment of a receptive endometrium. Poor endometrial receptivity has generally been considered as a major cause of infertility. Protein glycosylation is associated with many physiological and pathological processes. The fucosylation is catalyzed by the specific fucosyltransferases. Fucosyltransferase IV (FUT4) is the key enzyme for the biosynthesis of α1,3-fucosylated glycans carried by glycoproteins, and the previous studies showed FUT4 expressi ...[more]

PMID: 28914881

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Project description:Osteoarthritis (OA), characterized by the degeneration of articular cartilage, is a major problem in aging populations, and cartilage chondrocytes have been indicated to serve a curial role in the progression of OA. MicroRNA-200b-3p (miR-200b) was preliminarily identified to participate in OA. However, its role and mechanism of action in injured chondrocytes in OA remain unclear to date. In the present study, lipopolysaccharide (LPS)-treated cells isolated from normal knee articular cartilage were used to mimic inflammatory injury of OA chondrocytes. Cell viability, apoptosis and inflammatory responses were detected using Cell Counting Kit-8, flow cytometry and enzyme-linked immunosorbent assay, respectively. The expression levels of miR-200b and fucosyltransferase-4 (FUT4) were measured by reverse transcription-quantitative PCR and western blotting. The association between miR-200b and FUT4 was verified using TargetScan software, dual-luciferase reporter assay and RNA immunoprecipitation. The results indicated that LPS treatment decreased cell viability of primary chondrocytes, and increased apoptosis rate and production of IL-1β, IL-6 and TNF-α. The expression level of miR-200b was downregulated, and that of FUT4 was upregulated in OA cartilage tissues and LPS-treated normal chondrocytes compared with normal cartilage tissues and chondrocytes. Overexpression of miR-200b via transfection with miR-200b mimic inhibited the apoptosis rate and reduced the levels of IL-1β, IL-6 and TNF-α in LPS-stimulated chondrocytes. However, the suppressive effect of miR-200b overexpression on the LPS-induced inflammatory injury in chondrocytes was reversed by the restoration of FUT4 levels. Notably, FUT4 was indicated to be a downstream target of miR-200b and was negatively regulated by miR-200b. Taken together, the results of the current study indicated that miR-200b protected chondrocytes from LPS-induced inflammatory injury in vitro by targeting FUT4. These findings revealed the miR-200b/FUT4 axis as a potential candidate to target the degeneration of cartilages, thereby inhibiting the progression of OA.

Dataset Information

MicroRNA-200c impairs uterine receptivity formation by targeting FUT4 and ?1,3-fucosylation.

Publications

MicroRNA-200c impairs uterine receptivity formation by targeting FUT4 and α1,3-fucosylation.

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