Preeclampsia (PE) is a serious pregnancy complication characterized by hypertension and organ dysfunction. Its pathogenesis involves impaired trophoblast invasion and inadequate spiral artery remodeling; however, the underlying molecular mechanisms remain unclear. This study investigated the role of arylacetamide deacetylase (AADAC) in PE and its effects on trophoblast function by analyzing placental tissues from 30 patients with PE and 15 controls. Exploratory RNA sequencing was performed on pooled placental samples from six patients with severe PE and six controls, and AADAC expression was validated by semi-quantitative PCR and Western blotting. HTR8/SVneo cells were exposed to cobalt chloride (CoCl₂) under hypoxia-mimicking conditions, and AADAC expression was manipulated by siRNA-mediated knockdown (KD) and overexpression (OE). RNA sequencing revealed increased AADAC expression in PE placentas (fold change > 2.0, raw p < 0.05). Although AADAC mRNA levels were elevated in PE tissues, protein levels were reduced. CoCl₂ exposure was associated with increased expression of AADAC and hypoxia-inducible factor-1 alpha (HIF-1α). Under hypoxia-mimicking conditions, AADAC silencing was associated with increased trophoblast invasion and tube formation, whereas AADAC overexpression reduced tube formation without significantly affecting invasion. These findings suggest that dysregulated, hypoxia-responsive AADAC expression influences trophoblast invasive and angiogenic behavior in preeclampsia.

The purpose of this paper is to evaluate the association of maternal clinical and laboratory features and placental histopathological changes with disease severity in pregnancy-related hypertensive disorders. From January 2021 to December 2021, clinical and laboratory data at the time of delivery and histopathological features of the placenta were collected from pregnant women with pregnancy-related hypertensive disorders at a single institution. The women were classified according to the pregnancy-related hypertensive disorder clinical severity, and each variable was compared accordingly. Gestational age-matched normotensive groups were also compared. Univariate and multivariate regression analyses were used to identify factors influencing pregnancy-related hypertensive disorder severity. Fifty-eight pregnancies were analyzed. Maternal albumin levels before delivery (beta coefficient −0.83, p = 0.043) and increased placental syncytial knots (beta coefficient 0.71, p = 0.026) are important parameters that are closely related to disease severity in women with pregnancy-related hypertensive disorders. The combination of albumin, PAPP-A, total bilirubin, and eGFR levels appears to be optimal for predicting pregnancy-related hypertensive disorder severity.