Exploring the Role of miRNA-101a in the Circulatory System’s Adaptive Mechanisms in Hypertensive Disorders of Pregnancy

<b>Background/Objectives:</b> Hypertensive disorders of pregnancy constitute one of the principal reasons for maternal and perinatal morbidity and mortality worldwide. Identification of molecular mechanisms causing placental dysfunction resulting in gestational hypertension is crucial in the development of new methods of prevention and treatment. The aim of this case-control study was to assess changes in miRNA expression, and biomarkers such as NT-proBNP and galectin-3, in women with uncomplicated pregnancies and hypertensive disorders of pregnancy. <b>Methods:</b> This was a case-control study. We included 61 women with uncomplicated pregnancies and 31 women with hypertensive disorders of pregnancy (21 women with gestational hypertension and 10 women with chronic hypertension). Blood sample collection was performed at 33 weeks of gestation. Expression and expression levels of 26 microRNAs, NTproBNP, and galectin-3 were measured. <b>Results:</b> Lower expression of microRNA 101a was observed in patients with hypertensive disorders of pregnancy. The expression of microRNA 101a was significantly lower in the group of patients with gestational hypertension, but not with chronic hypertension. Not only was the expression of microRNA 101a lower in all women with gestational hypertension but also in XYZ% it reached undetectable levels. Other studied microRNAs were similar in expression and concentration levels among both groups. In all women with hypertensive disorders of pregnancy, statistically significant correlations were detected between NT-proBNP concentrations and microRNA 133a (r = -0.68; <i>p</i> = 0.030) and microRNA 195 (r = 0.67; <i>p</i> = 0.030), and between galectin-3 and microRNA 195 (r = 0.46; <i>p</i> = 0.010), microRNA 133a (r = 0.44; <i>p</i> = 0.020), microRNA 222-2276 (r = 0.39; <i>p</i> = 0.050). <b>Conclusions:</b> microRNA 101a, a molecule associated with placental dysfunction in preeclampsia and with inhibition of cardiac fibrosis, has lower expression and concentration levels in gestational hypertension but not in chronic hypertension.