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Impact of gestational and type 2 diabetes on fetal endothelial cell miRNA expression
1Medical Laboratory Sciences, Faculty of Applied Medical Sciences, King Abdulaziz University, Jeddah, Saudi Arabia; Regenerative Medicine Unit, King Fahad Medical Research Center, King Abdulaziz University, Jeddah, Saudi Arabia.
Aims:
Fetal exposure to hyperglycemia in utero have been suggested to induce epigenetic changes through expression of various miRNAs, and cause dysfunctional endothelium connected with elevated risk of cardiovascular disease (CVD) in offspring during early adulthood. In this study, we investigated whether hyperglycemia-induced changes in the expression of 28 fetal endothelial microRNAs (miRNAs) are associated with endothelial dysfunction and CVD.
Methods:
Differentially expressed miRNAs in TaqMan miRNA human arrays were quantified using qPCR.
Results:
The expression of miR-140-3p, miR-1307-5p, miR-342-3p, and miR-16-5p was significantly reduced in human umbilical vein endothelial cells (HUVECs) from females with gestational diabetes (GDM-UVECs) compared with that of the control group. Meanwhile, in type 2 diabetes (T2D-HUVECs), miR-126-3p and miR-27a-5p were significantly reduced, while miR-27b-3p was significantly increased. Furthermore, miR-29b-3p expression was upregulated in both GDM- and T2D-HUVECs compared with that in the control. The expression of fibroblast growth factor 11 (FGF11) mRNA-a target of dysregulated miR-342-3p-was downregulated in GDMHUVECs compared with that in the control.
Conclusions:
Altered miRNA and target FGF11 mRNA expression may contribute mechanistically to endothelial dysfunction in diabetic HUVECs when maintained under normal glucose conditions for several passages.
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