The role of cholesterol/ALKBH1/ITGA2B in thrombosis in placental vessels of preeclampsia
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ABSTRACT:
PROVIDER: PRJNA1227461 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR32467234_1.fastq.gz | Fastqsanger.gz | |||
| SRR32467234_2.fastq.gz | Fastqsanger.gz | |||
| SRR32467235_1.fastq.gz | Fastqsanger.gz | |||
| SRR32467235_2.fastq.gz | Fastqsanger.gz | |||
| SRR32467236_1.fastq.gz | Fastqsanger.gz |
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Project description: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.
2025-03-06 | GSE290312 | GEO
Project description:Preeclampsia is a severe placenta-related pregnancy disorder that is generally divided into two subtypes named early-onset preeclampsia (onset <34 weeks of gestation), and lateonset preeclampsia (onset ≥34 weeks of gestation), with distinct pathophysiological origins. Both forms of preeclampsia have been associated with maternal systemic inflammation. However, alterations in the placental immune system have been less well characterized. Here, we studied immunological alterations in early- and late-onset preeclampsia placentas using a targeted expression profile approach. RNA was extracted from snap-frozen placenta samples (healthy n=13, early-onset preeclampsia n=13, and late-onset preeclampsia n=6). The expression of 730 immune-related genes from the Pan Cancer Immune Profiling Panel was measured, and the data were analyzed Q10 in the advanced analysis module of nSolver software (NanoString Technology). The results showed that early-onset preeclampsia placentas displayed reduced expression of complement, and toll-like receptor (TLR) associated genes, specifically TLR1 and TLR4. Mast cells and M2 macrophages were also decreased in early-onset preeclampsia compared to healthy pl acentas. The findings were confirmed by an immunohistochemistry approach using 20 healthy, 19 early-onset preeclampsia, and 10 late-onset preeclampsia placentas. We conclude that the placental innate immune system is altered in early-onset preeclampsia compared to uncomplicated pregnancies. The absence of these alterations in late-onset preeclampsia placentas indicates dissimilar immunological profiles. The study revealed distinct pathophysiological processes in earlyonset and late-onset preeclampsia placentas and imply that a tailored treatment to each subtype is desirable.
2021-12-13 | GSE190639 | GEO
Project description:AlkB homolog 1 (ALKBH1) has been reported to act as a DNA 6mA demethylase to remove 6mA modificatione in ukaryotic genomes. Our previous data showed downregalted ALKBH1 in mouse and human fatty liver and increased DNA 6mA levels in mouse fatty liver. We hypothesize that ALKBH1 may be involved in hepatic lipid metabolism. To test this hypothesis, we generated liver-specific ALKBH1 knockout (Alkbh1 f/f, Albumine-cre; AKO) mice and used high-throughput RNA sequence and other assays to directly study the role of ALKBH1 during the development of hepatic steatosis.
2022-10-26 | GSE193497 | GEO
Project description:The series is composed of thirty hybridizations for analysis of differentially expressed genes in normal placenta tissues from patients with normal labor and placenta tissues from patients with severe preeclampsia. Patients tissues samples were obtained from (Vasilis. Total RNA extraction was performed by using the MagNa Pure Compact RNA Isolation Kit (Roche Applied Science). Keywords: Gene expression study, Disease state Twenty-six out of 50 normal placentas were randomly selected to match with 17 preeclamptic placentas, accounting for parity. Microarrays were performed applying a direct comparison design.
2010-05-26 | E-GEOD-10588 | biostudies-arrayexpress
Project description:Analysis of genome-wide gene expression in placentas from women with preterm severe preeclampsia, with or without HELLP syndrome, compared to gestational age-matched controls. The hypothesis tested in the present study was that placental transcriptomic changes in preeclampsia are considerably different from controls. The results provide important information on placental transcriptomic changes in preeclampsia.
2018-12-30 | GSE66273 | GEO
Project description:We perform placental microRNA expression profiling to identify potential microRNAs involved in the development and pathogenesis of preeclampsia. microRNA expression profiling for serum was quantified by qPCR and evaluated at 12, 16, and 20 gestational weeks and at the time of preeclampsia diagnosis. Two groups were evaluated using TaqMan Low Density Array plates: a control group with 18 normotensive pregnant women and a preeclampsia group with 16 patients who developed preeclampsia during the follow-up period. The placental microRNA profile was assayed at delivery (7 cases and 7 controls) using the Illumina GAIIx sequencing platform.
2015-06-03 | GSE69452 | GEO
Project description:DNA N6-methyladenosine (6mA) in eukaryotic genomes has recently been observed in diverse species. 6mA has been reported to associate with multiple physiological processes including embryonic development and tumorigenesis, and ALKBH1 is a primary 6mA demethylase in mouse and human cells. To research the roles of 6mA and its putative regulators such as putative ALKBH1 in the homeostatic maintenance of human stem cells and their differentiated derivatives, We generated ALKBH1-deficient human embryonic stem cells (hESCs) via CRISPR/Cas9-mediated non-homologous end joining (NHEJ). We next differentiated ALKBH1+/+ and ALKBH1-/- hESCs into human mesenchymal stem cells (hMSCs) and vascular smooth muscle cells (hVSMCs). Early-onset growth arrest of ALKBH1-/- hMSCs was observed, and increased apoptosis and enhanced migration ability were observed in ALKBH1-/- hVSMCs. However, liquid chromatography coupled with tandem mass spectrometry (LC-MS/MS) analysis revealed no change in 6mA levels between ALKBH1+/+ and ALKBH1-/- hESCs, between ALKBH1+/+ and ALKBH1-/- hMSCs, and between ALKBH1+/+ and ALKBH1-/- hVSMCs, respectively. These data demonstrate that depletion of ALKBH1 exerts minimal impact on 6mA levels in hESCs and their differentiated derivatives and that ALKBH1 regulates the homeostasis of hMSCs and hVSMCs possibly in a DNA 6mA-independent manner.
2020-05-22 | GSE150936 | GEO
Project description:Dysregulated RNA editing is well documented in several diseases such as cancer. The extent to which RNA editing might be involved in diseases originated in the placenta such as preeclampsia remains unknown, because RNA editing has rarely been studied in the placenta. Here, the RNA editome is systematically profiled on placentae from 9 patients with early-onset severe preeclampsia (EOSPE) and 32 normal controls, and a widespread RNA editing dysregulation in EOSPE has been identified. The mis-edited gene set is enriched with known preeclampsia-associated genes and differentially expressed genes in EOSPE. The “RNA editing events” at two microRNA binding sites in 3’-UTR of the LEP mRNA have been generated, which leads to increased expression level of LEP in trophoblast cells. Upregulation of LEP is also observed in the placentae of PE patients. These results suggest that widespread placental RNA editing may be involved in placental development and dysregulation of RNA editing in the placenta may contribute to the pathogenesis of preeclampsia.
2020-04-20 | GSE148241 | GEO
Project description:Placental Immune alterations in early-onset preeclampsia and late-onset preeclampsia
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Project description:The series is composed of thirty hybridizations for analysis of differentially expressed genes in normal placenta tissues from patients with normal labor and placenta tissues from patients with severe preeclampsia. Patients tissues samples were obtained from (Vasilis. Total RNA extraction was performed by using the MagNa Pure Compact RNA Isolation Kit (Roche Applied Science). Keywords: Gene expression study, Disease state
2008-06-20 | GSE10588 | GEO