## 1 Introduction  
Preeclampsia (PE) is a specific disease in pregnancy which can have serious implications, being a leading cause of fetal and maternal morbidity and mortality [1; 2]. According to a World Health Organization (WHO) systematic analysis performed in 2014, hypertensive disorders in pregnancy were the second cause of maternal death after hemorrhage, accounting for 14% of such cases worldwide [3]. In mothers with acute renal and liver dysfunction, pulmonary edema and brain edema could be observed [4]. The etiology of preeclampsia is complex and not fully understood. Currently, it is assumed that this disorder is based on processes that lead to a disturbed process of placentation [5]. Many studies have shown that the occurrence of PE is associated with a reduced vitamin D (VD) level [6]. Moreover, most scientific societies recommend VD supplementation during pregnancy due to its widespread deficiency in the population of pregnant women [7; 8; 9] and the potential relationship of VD deficiency with occurrence of obstetric complications [10; 11]. In the placenta, especially in the syncyotrophoblast, the expression of genes related to the vitamin D pathway, such as 25-hydroxylase (CYP2R1), 1\(\alpha\)-hydroxylase (CYP27B1), and 24-hydroxylase (CYP24A1), has been described, which guarantees efficient VD metabolism in pregnant women. These hydroxylases play an important role in the conversion of cholecalciferol to calcitriol, which is the active form of vitamin D (1,25(OH)\({}_{2}\)D\({}_{3}\), 1,25-D\({}_{3}\)). Alterations in expression and activity of hydroxylases could disturb the circulating VD level. The plasma concentration of calcitriol increases 2-3 times in pregnant women compared to the level before pregnancy, starting at 10-12 weeks of gestation and continuing until the end of pregnancy [12]. The VD augmentation is independent of the parathyroid hormone, the level of which remains unchanged throughout pregnancy [13]. In humans, vitamin D manifests a pleiotropic function and acts on target organs, specifically binding to the vitamin D receptor (VDR). The important action of vitamin D in pregnancy has a combined influence in both mother and fetus. Experimental studies have shown that both the 1,25(OH)\({}_{2}\)D\({}_{3}\) form and its precursor 25(OH)D increase trophoblast invasion in vitro [14]. In the human syncyotrophoblast, calcitriol in an autocrine manner regulates the synthesis of human chorionic gonadotropin (hCG) [15], human placental lactogen (hPL) [16], estradiol, and progesterone [17]. The vitamin D receptor (VDR) belongs to a family of nuclear steroid receptors and, as a nuclear transcription factor, binds to the retinoid X receptor (RXR). This complex recognizes the vitamin D responsive elements (VDREs) in the DNA promoter sequence of genes regulated directly by vitamin D [18]. The expression of VDR is influenced by co-activators and co-repressors, which enhance or inhibit gene expression, respectively. Co-receptors bind to the VDR and block its activity in the absence of a ligand. According to the multipotential action of vitamin D, even VDRs have been located in many tissues of the human body [19; 20]. It was demonstrated conclusively that the proper VD level during pregnancy and appropriate placental expression of genes linked to the VD pathway are crucial for the growth and function of the placenta [21]. On the other hand, several studies have shown that vitamin D deficiency could be strongly associated with preeclampsia development [22; 23; 24; 25]. This fact may be related to changes in VDR and hydrolase placental expression, which disturb VD metabolism in preeclamptic women. Additionally, the abnormal trophoblast invasion in early pregnancy and disturbing placental angiogenesis are connected with the development of PE. Considering the above observations, we hypothesized that expression of VDR and several hydrolase genes, as well as proteins, in preeclamptic placentas would differ from those in physiological pregnancies [5].