Abstract
Gestational diabetes mellitus (GDM) is a metabolic dysregulation closely related to both obesity and type 2 diabetes; however, the molecular mechanism underlying GDM is still unclear. The purpose of this study was to investigate the effects of microRNA-377 (miR-377-3p) and fibronectin type III domain containing 5 (FNDC5) in regulating the cell growth of trophoblasts under high glucose (HG) conditions during the development of GDM. Serum miR-377-3p was upregulated and positively correlated with fasting blood glucose level in GDM patients. miR-377-3p downregulation increased the cell vitality and suppressed the cell apoptosis of HG-treated HTR-8/SVneo and BeWo cells. Using TargetScan prediction, luciferase assay, and western blot, it was found that miR-377-3p could target FNDC5 and suppress its expression. However, FNDC5 downregulation abolished the effect of miR-377-3p inhibitor in HTR-8/SVneo cells. Together, miR-377 is a potential target for GDM biomarker, which promotes cell growth and suppresses cell apoptosis, partly through the upregulation of FNDC5.
Highlights
Gestational diabetes mellitus (GDM) is a metabolic dysregulation closely related to both obesity and type 2 diabetes [1]
Studies have shown that high glucose (HG) can induce human umbilical vein endothelial cell dysfunction via upregulation of miR-137 levels in gestational diabetes [5]. miR-657 promoted macrophage polarization to M1 by targeting FAM46C in gestational diabetes [6]. miR-137 restricts the survival and migration of human chorionic trophoblast cells HTR-8/ SVneo cells by decreasing fibronectin type III domain containing 5 (FNDC5) in gestational diabetes [7]. miR503 is upregulated in placental tissues and peripheral blood of GDM patients, and miR-503 can target FNDC5 to disrupt the function of islet cells [8]
A positive correlation between relative level of miR-377-3p and fasting blood glucose level in GDM patients was found (Figure 1b), which suggested that miR-377-3p might play an important role in the pathogenesis of GDM
Summary
Gestational diabetes mellitus (GDM) is a metabolic dysregulation closely related to both obesity and type 2 diabetes [1]. The role of some miRNAs in gestational diabetes has recently been found [4]. Studies have shown that high glucose (HG) can induce human umbilical vein endothelial cell dysfunction via upregulation of miR-137 levels in gestational diabetes [5]. MiR-137 restricts the survival and migration of human chorionic trophoblast cells HTR-8/ SVneo cells by decreasing fibronectin type III domain containing 5 (FNDC5) in gestational diabetes [7]. MiR503 is upregulated in placental tissues and peripheral blood of GDM patients, and miR-503 can target FNDC5 to disrupt the function of islet cells [8]. Studies have shown that miR-377-3p overexpression can upregulate the level of fibronectin in diabetic nephropathy [9]. The role and mechanism of miR-377-3p in gestational diabetes have not been reported
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