Placental Privilege: Evidence of Organ Resilience in severe COVID-19
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE249139 | GEO | 2025/03/28
REPOSITORIES: GEO
Similar Datasets
Project description:Placental Privilege: Evidence of Organ Resilience in severe COVID-19
| PRJNA1047537 | ENA
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:Severe SARS-CoV-2 infection causes COVID-19. The host response to SARS-CoV-2 is poorly understood partly due to a lack of an animal model that recapitulates severe manifestations of human disease. Here we report a Syrian hamster model that develops a rapidly progressive lethal pulmonary disease that closely mimics human severe COVID-19. We evaluated host responses to infection using a multi-omics, multi-organ approach to define kinetic changes to the proteome, the phospho-proteome, and the transcriptome. These data revealed a robust antiviral response composed of both Type I and Type II interferon responses at the gene and protein levels. Both IFN and TNF-a responses were associated with peak viral replication at day 2 post-infection. These responses correlated to rapidly developing diffuse alveolar destruction and pneumonia that persisted in the absence of active viral infection. Extrapulmonary viral replication was detected in the heart and kidneys, which correlated with proteome and phospho-proteome remodeling in each organ. In addition to early antiviral responses, there was a significant and progressive increase in chemokines, monocyte, and neutrophil-associated molecules throughout the course of infection that peaked in the later time points. Together, our results provide a kinetic overview of multi-organ host responses to severe SARS-CoV-2 infection in vivo.
2021-02-22 | MSV000086925 | MassIVE
Project description:DNA microarray was applied to characterize the whole-genome expression profiles of placentas during ICP development. Pregnant women were categorized evenly into three groups: healthy group; mild ICP, with serum bile-acid concentration ranging from 10M-bM-^@M-^S40 uM; and severe ICP, with bile-acid concentration >40 uM.
2013-04-18 | E-GEOD-46157 | biostudies-arrayexpress
Project description:Pre-eclampsia is one of the most serious pregnancy-associated disorders, and is defined by hypertension (systolic blood pressure higher than 140mmHg or diastolic blood pressure higher than 90mmHg) with proteinuria (more than 0.3g/day). It is not a simple complication of pregnancy, but is rather a syndrome of multiple organ failure involving the liver, kidney, and lung, as well as coagulatory and neural systems. There is now an emerging consensus that pre-eclampsia is a complex polygenetic trait in which maternal and fetal genes, as well as environmental factors, are involved, although the precise mechanism of the disorder has remained elusive. In this study, we have performed gene expression profiling to further elucidate the mechanisms underlying the development of the pre-eclamptic condition. We thus compared the expression profiles in placentas from women who underwent a normal pregnancy and from women suffering from severe pre-eclampsia. In addition, we compared the expression data between the early and late onset forms of pre-eclampsia and obtained a number of potential new prognostic biomarkers for this disease. Keywords: disease state analysis
2006-04-25 | GSE4707 | GEO
Project description:Paternally expressed 11/Retrotransposon-like 1 (Peg11/Rtl1) knockout (KO) mice exhibited mid to late fetal lethality or late fetal growth retardation associated with frequent neonatal lethality. The lethal phenotype was largely dependent on genetic background and became more severe with each succeeding generation in the course of backcross experiments to C57BL/6 (B6). We previously suggested these lethal and growth phenotypes were due to severe defects in placental fetal capillaries in labyrinth layer. In this study, we reexamined KO fetuses exhibiting mid fetal lethality with internal bleeding. Importantly, basal region of fetal capillary network was specially damaged, therefore, also leading to poor expansion of the labyrinth layer and placental size reduction in later stage. Apparent up-regulation of Guanine nucleotide binding protein, alpha 2 (Gnai2) and decrement of Transmembrane protein 100 (Tmem100), Mesenchyme homeobox 2 (Meox2) and Lymphatic vessel hyaluronan Receptor 1 (LYVE1) expression were observed in earlier stage of placentas even before apparent morphological changes occurred, suggesting that these genes are involved in the maintenance of fetal capillaries associated with Peg11/Rtl1 in development.
2016-10-19 | GSE88849 | GEO
Project description:Paternally expressed 11/Retrotransposon-like 1 (Peg11/Rtl1) knockout (KO) mice exhibited mid to late fetal lethality or late fetal growth retardation associated with frequent neonatal lethality. The lethal phenotype was largely dependent on genetic background and became more severe with each succeeding generation in the course of backcross experiments to C57BL/6 (B6). We previously suggested these lethal and growth phenotypes were due to severe defects in placental fetal capillaries in labyrinth layer. In this study, we reexamined KO fetuses exhibiting mid fetal lethality with internal bleeding. Importantly, basal region of fetal capillary network was specially damaged, therefore, also leading to poor expansion of the labyrinth layer and placental size reduction in later stage. Apparent up-regulation of Guanine nucleotide binding protein, alpha 2 (Gnai2) and decrement of Transmembrane protein 100 (Tmem100), Mesenchyme homeobox 2 (Meox2) and Lymphatic vessel hyaluronan Receptor 1 (LYVE1) expression were observed in earlier stage of placentas even before apparent morphological changes occurred, suggesting that these genes are involved in the maintenance of fetal capillaries associated with Peg11/Rtl1 in development.
2016-10-19 | GSE88891 | GEO
Project description:Robust identification of placental PPARg target genes via mutliple PPARg-dependence criteria. Integration of differential expression data from Pparg-null, Rxra-null, Med1-nul and Ncoa6-null placentas and from WT and Pparg-null Trophoblast stem cells (TSC) differentiated for 2 or 4 days in the presence or absence of the PPARg agonist Rosiglitazone (Rosi). [Placentas] Three pools of three WT placentas, each vs a litter-matched pool of three Pparg-null placentas Three pools of three WT placentas, each vs a litter-matched pool of three Rxra-null placentas Three pools of three WT placentas, each vs a litter-matched pool of three Med1-null placentas Three pools of three WT placentas, each vs a litter-matched pool of three Ncoa6-null placentas [Trophoblast stem cells (TSC)] Three independent WT TSC lines differentiated for two and four days in the presence or absence of Rosi vs two independent Pparg-null TSC lines differntiated for the same durations in the presence of Rosi
2012-07-09 | E-GEOD-39233 | biostudies-arrayexpress
Project description:The study aims at investigating the specifical transcriptional signatures of severe COVID-19
2021-01-15 | GSE164805 | GEO