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The role of cholesterol/ALKBH1/ITGA2B in thrombosis in placental vessels of preeclampsia

ABSTRACT: The risk of multiple placental thrombosis is increased in preeclampsia (PE) and vascular endothelium plays vital roles in coagulation such as secreting ITGA2B, vWF and TF. However, the pathological mechanism is unclear. Placental blood vessels were collected from PE and normal pregnancies. The protein level of ITGA2B was up-regulated in PE compared to the control, indicating enhanced coagulation function in the placenta of PE. Higher cholesterol levels and lower ALKBH1 expression were found in placental blood vessels of PE while the whole DNA N6-methyldeoxyadenosine levels (6mA) were up-regulated. However, DNA 6mA level of ITGA2B promoter was decreased. The Cholesterol overload experiment in human umbilical vein endothelial cells (HUVECs) showed that cholesterol regulated the protein expressions of ALKBH1 and ITGA2B, which was related to cholesterol concentration. ITGA2B protein expression was increased after ALKBH1 knockout. These data provide important information on cholesterol levels, ALKBH1 and ITGA2B expressions in coagulation function in placental blood vessels, which may be helpful for further investigations of potential targets and early prevention of placental thrombosis in PE.

ORGANISM(S): Homo sapiens

PROVIDER: GSE290312 | GEO | 2025/03/06

REPOSITORIES: GEO

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Project description:Background: Preeclampsia (PE) is a placental disease characterized by hypertension and proteinuria in pregnant women, which is associated with a high maternal and infantile morbidity. However, circulating biomarkers able to predict the prognosis of PE are lacking. Methods: Thirty-eight women were included in the study. They consisted of 19 patients with PE (13 with severe PE and 6 women with non-severe PE) and 19 gestational age-matched normal pregnancy controls. We measured coagulation pathway, endothelial responses and microparticle release and circulating gene expression in PE patient groups and normotensive controls. Results: The measurement of markers associated with coagulation pathway, endothelial activation and circulating microparticles enabled to discriminate PE from normal pregnancy but were not sufficient to distinguish severe from non-severe PE. PE patients also exhibited a specific transcriptional program distinct from that of control women and subtle differences were observed between severe and non-severe PE. Functional annotation of the up-modulated signature in PE highlighted two main functions related to ribosome and complement. Importantly, we found that 8 genes were specifically up-modulated in severe preeclampsia. Among these genes, the expression of VSIG4 was significantly increased in patients with severe preeclampsia in comparison with controls and patients with non-severe preeclampsia. Conclusion: Using transcriptional signatures of blood samples, we identified the gene encoding the estrogen receptor as a potential diagnostic marker of severe preeclampsia. In addition, the determination of this gene may improve the prognostic assessment of severe preeclampsia. Thirty-eight women were included in the study: 19 patients with PE, including 6 women with non-severe PE and 13 with severe PE, and 19 women with normal pregnancy (NP) selected according to age, weight, smoking status, race, gestational age at the inclusion, and blood pH (Table 1 of manuscript). Women with NP had no history of medical illness or medication, and received routing prenatal care. The diagnostic of PE was based on a blood pressure of M-bM-^IM-% 140/90 mmHg taken twice, uricemia above normal laboratory range (120-420 M-BM-5mol/L), and proteinuria higher than 300 mg in a 24 hour-collection, occurring after 20 gestational weeks in previously normotensive women (Table 2). The criteria used to define severe PE included one of the following conditions: a blood pressure higher than 160/110 mmHg, a proteinuria higher than 1500 mg/24h), a multisystem disorder, maternal cerebral symptoms (seizures, stroke) or intrauterine growth restriction below the 3M-BM-0 percentile. Women with multiple gestations, fetal congenital malformations/chromosomal abnormalities, recent infection, antiphospholipid antibodies, trauma, drug or alcohol abuse during pregnancy, preexisting hypertension, thrombophilia with PE history, or women receiving anticoagulant or antiaggregation therapy were excluded from the study. Two microarrays (one non-severe PE and one normal) were discarded from the analysis for technical reasons. Thus, only 36 microarrays are included here.

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The role of cholesterol/ALKBH1/ITGA2B in thrombosis in placental vessels of preeclampsia

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