Fetal Microsatellite in the Heme Oxygenase 1 Promoter Is Associated With Severe and Early-Onset Preeclampsia

Abstract

Preeclampsia is a vascular pregnancy disorder that often involves impaired placental development. HO-1 (heme oxygenase 1, encoded by ) is a stress response enzyme crucial for endothelial and placental function. Long version of the guanine-thymine (GT) microsatellite in the promoter decreases HO-1 expression, and the long maternal repeat is associated with late-onset preeclampsia. Our aim was to study whether the length of fetal repeat is associated with mother's preeclampsia, whether the length of fetal and maternal repeats affect HO-1 levels in placenta and maternal serum, and whether HO-1 levels are altered in preeclampsia. We genotyped the repeat in the cord blood of 609 preeclamptic and 745 nonpreeclamptic neonates. HO-1 levels were measured in 36 placental samples, and in the first (222 cases/243 controls) and third (176 cases/53 controls) pregnancy trimester serum samples using enzyme-linked immunosorbent assay. The long fetal GT repeat was associated with preeclampsia and its severe and early-onset subtypes. Interaction analysis suggested the maternal and fetal effects to be independent. Placental or serum HO-1 levels were not altered in preeclamptics, possibly reflecting heterogeneity of preeclampsia. Carriers of the long fetal and maternal repeats had lower placental and serum HO-1 levels, respectively, providing functional evidence for the association. We conclude that the long fetal GT repeat may increase mother's risk for especially severe and early-onset preeclampsia. The fetal and maternal risk alleles likely predispose to different disease subtypes.

MZe786 Rescues Cardiac Mitochondrial Activity in High sFlt-1 and Low HO-1 Environment

“…Likewise, the partial deletion of Hmox1 also leads to signs of intrauterine growth restriction [63]. In humans, the variation in maternal and fetal microsatellites in the Hmox1 promoter is likely to predispose women to preeclampsia during pregnancy [64]. In the present study, Hmox1 deficiency resulted in the suppression of the mitochondrial activity and reduced PGC1-α gene expression in the heart.…”

MiR-101-containing extracellular vesicles bind to BRD4 and enhance proliferation and migration of trophoblasts in preeclampsia

“…PE is a vascular disease that occurs during pregnancy and results in the impairment of placental development [21]. The differentiation of trophoblasts in the placenta could form the multinuclear layer-covering placenta, playing an essential role in the etiology of PE [22].…”

Simulation and Analysis of Perturbation and Observation-Based Self-Adaptable Step Size Maximum Power Point Tracking Strategy with Low Power Loss for Photovoltaics

“…According to Figure 19 and the parameters of the PV module shown in Table 2, the power loss can be calculated using the equation expressed in the Methods section of this report. According to Equations (8) and (11), the steady-state power loss of the conventional P&O tactic is calculated as follows. According to Equations (8) and (11), the steady-state power loss of the conventional P&O tactic is calculated as follows.…”

“…According to Equations (8) and (11), the steady-state power loss of the conventional P&O tactic is calculated as follows. According to Equations (8) and (11), the steady-state power loss of the conventional P&O tactic is calculated as follows. P L P MPP conventianl ≈ 0.69% (16) According to Equations (8) and (13), the steady-state power loss of the conventional P&O tactic is given as follows.…”

“…For example, increasing the temperature results in a slight increase in the short-circuit current and a significant decrease in the open-circuit voltage, which reduces the maximum output power. maximum output point called the maximum power point (MPP) [7,[11][12][13][14][15][16][17][18][19][20][21][22]. For the PV system operated with higher efficiency, an MPP tracking (MPPT) controller is indispensable; the tracking methodologies are introduced in detail in the MPPT section of this report.…”