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Preeclampsia (PE) is a pregnancy-related hypertensive disorder that affects 5-8% of all pregnancies worldwide. Placental microRNA (miRNA) expression is known to be dysregulated during PE which includes miR-210. However, the role of miR-210 in the development of PE is still unknown. We have previously demonstrated STAT6, a transcription factor, to be a direct target of miR-210. In addition, STAT6 modulates levels of IL-4, an anti-inflammatory cytokine which is known to be beneficial during pregnancy. Given that the STAT6/IL-4 pathway is important for normal pregnancy, we hypothesized that an overexpression of miR-210 in mice will contribute to PE-like symptoms by inhibiting the STAT6/IL-4 pathway. Systolic blood pressures (SBP) were measured using the tail-cuff method on both WT (C57Bl/6J) and miR-210 TG mice. The miR-210 TG mice exhibited increased SBP compared to the WT mice (WT: 95±2 mmHg, miR-210 TG: 115±2.4 mmHg, p

Preeclampsia (PE) is an obstetric complication that is diagnosed by hypertension and proteinuria at or after 20 weeks of gestation. PE is a multifactorial disease, but it is widely accepted that impaired proangiogenic factors such as vascular endothelial growth factor (VEGF), placental growth factor (PlGF) and antiangiogenic factor such as soluble FMS-like tyrosine kinase-1 (sFlt1) or VEGF receptor-1 balance during pregnancy is linked to PE. sFlt1, a splice variant of Flt1 binds to either VEGF or PlGF and blocks their action. In addition, placental angiogenesis is known to be regulated by specific miRNAs that are typically dysregulated during PE highlighting the importance of these miRNAs in pregnancy disorders. miR-210 is upregulated in placentas and serum/plasma of PE women and is also known to modulate angiogenic pathways. Therefore, we hypothesized that miR-210 overexpression contributes to the development of PE-like symptoms by altering the angiogenic/antiangiogenic pathway. To this end, we demonstrate increased systolic blood pressure (SBP: miR-210 TG P = 115 ± 2 mm Hg vs. WT P = 95 ± 2 mm Hg, p