Figure 9.

Schematic diagram showing that NF-κB–responsive miR-31-5p contributes to the pathogenesis of preeclampsia. miR-31-5p up-regulated by activation of NF-κB under inflammatory conditions inhibits post-translational regulation of eNOS expression, leading to the decreased NO production. The decreased NO bioavailability impairs endothelial cell (EC) function associated with angiogenesis (vascular remodeling), vascular smooth muscle cell (SMC) activity responsible for vascular relaxation via dysregulation of the sGC/cGMP pathway, and trophoblast invasion (spiral artery remodeling) by decreasing cGMP production. These events contribute to the pathogenesis of preeclampsia.