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Curr Mol Med. 2019;19(7):494-505. doi: 10.2174/1566524019666190520100422.

MiR-137 Restricts the Viability and Migration of HTR-8/SVneo Cells by Downregulating FNDC5 in Gestational Diabetes Mellitus.

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Department of Gynecology and Obstetrics, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, 600 Yishan Road, Shanghai 200233, China.
Laboratory for Reproductive Immunology, Shanghai Key Laboratory of Female Reproductive Endocrine Related Diseases, Obstetrics and Gynecology Hospital of Fudan University, Shanghai 200011, China.
Key Laboratory of Reproduction Regulation of NPFPC, SIPPR, IRD, Fudan University, Shanghai 200032, China.



An increasing number of studies have described the pathological changes of placenta tissues in gestational diabetes mellitus (GDM), although the underlying mechanisms involved in this process remain uncertain. The aim of the present study was to verify the possible role of microRNA-137 (miR)-137 and FNDC5 in regulating the biological function of trophoblasts in high glucose (HG) conditions during the GDM period.


Expression levels of miR-137 and FNDC5 were measured in placenta specimens, the HG-treated trophoblast cell line HTR-8/SVneo and miR-137- overexpressing HTR-8/SVneo cells using reverse transcription quantitative-PCR or western blotting. The viability of HTR-8/SVneo cells was tested using a Cell Counting kit- 8 (CCK8) assay, with cell migration assessed using scratch and transwell assays.


It was observed that the expression levels of miR-137 were increased and the expression levels of FNDC5 were decreased in the placenta tissues of women with severe GDM and in HG-exposed HTR-8/SVneo cells. In addition, upregulating miR-137 in HTR-8/SVneo cells downregulated the expression levels of FNDC5. The viability and migration of HTR-8/SVneo cells were suppressed by increased miR-137 expression levels, and upregulating FNDC5 in miR-137-overexpressing HTR-8/SVneo cells resulted in the reversal of all these effects.


The data from the present study suggest that miR-137 suppresses the viability and migration of trophoblasts via downregulating FNDC5 in GDM, which may contribute to the pathology of placenta tissues and occurrence of adverse pregnancy outcomes.


FNDC5; HTR-8/SVneo Cells; gestational diabetes mellitus; high glucose (HG).; miR-137; trophoblast cells.

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