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MiR-137 restricts viability and migration of HTR-8/SVneo cells by downregulating FNDC5 in gestational diabetes mellitus.

INTRODUCTION
Increasing number of studies have reported pathological changes of placenta tissues in gestational diabetes mellitus (GDM), while the underlying mechanisms involved in this process are still largely uncertain. Aim of the study is to verify the possible role of microRNA (miR)-137 and FNDC5 in regulating biological function of trophoblast cells in high glucose (HG) condition during GDM period.


METHODS
Expression of miR-137 and FNDC5 were measured in placenta specimens, HG treated trophoblast cell line HTR-8/SVneo and miR-137 overexpressed HTR-8/SVneo cells by quantitative real-time PCR or western blotting assay. And the viability of HTR-8/SVneo cells were tested by Cell Counting kit-8 (CCK8) assay, with migration ability of cells being detected by both scratch and transwell assay.


RESULTS
We observed that level of miR-137 augmented and expression of FNDC5 dampened in both placenta tissues of severe-GDM women and HG-exposed HTR-8/SVneo cells, and upregulating miR-137 in HTR-8/SVneo cells could downregulate level of FNDC5. The viability and migration of HTR-8/SVneo cells were suppressed by increased miR-137, and upregulating FNDC5 in miR-137 overexpressed HTR-8/SVneo cells could recover all these effects.


CONCLUSION
These data suggest that miR-137 suppresses viability and migration of trophoblasts via downregulating FNDC5 in GDM, which might contribute to pathology of placenta tissues and occurrence of adverse pregnancy outcomes.