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Longitudinal multi-omics identifies responses of megakaryocytes, erythroid cells and plasmablasts as hallmarks of severe COVID-19 trajectories [methylation]

ABSTRACT: Longitudinal multi-omics identifies responses of megakaryocytes, erythroid cells and plasmablasts as hallmarks of severe COVID-19 trajectories [methylation]

PROVIDER: PRJNA679336 | ENA |

REPOSITORIES: ENA

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Longitudinal multi-omics identifies responses of megakaryocytes, erythroid cells and plasmablasts as hallmarks of severe COVID-19 trajectories

Project description:Longitudinal multi-omics identifies responses of megakaryocytes, erythroid cells and plasmablasts as hallmarks of severe COVID-19 trajectories

| PRJNA679334 | ENA

Longitudinal multi-omics identifies responses of megakaryocytes, erythroid cells and plasmablasts as hallmarks of severe COVID-19 trajectories [sequencing]

Project description:Longitudinal multi-omics identifies responses of megakaryocytes, erythroid cells and plasmablasts as hallmarks of severe COVID-19 trajectories [sequencing]

| PRJNA679331 | ENA

Longitudinal multi-omics identifies responses of megakaryocytes, erythroid cells and plasmablasts as hallmarks of severe COVID-19 trajectories [sequencing]

Project description:In order to characterise the temporal dynamics of host response during COVID-19, we performed a longitudinal multi-omics study using a two centre German cohort of 13 patients. Bulk RNA was extracted from peripheral blood sampled at up to 5 time points per patient. At each sample point, a patient’s disease trajectory, “pseudotime”, was categorised according to clinical parameters. Both, whole transcriptome and B cell receptor sequence analysis was used to determine signatures specific to different disease trajectories. We identified coexpression modules that were associated with specific patterns across different COVID-19 disease trajectories. One module identified was related to failing interferon I response at the peak of disease severity. A second module showed biphasic upregulation of transcripts associated with erythropoiesis. Bulk BCR identified expansion of IgA+ and IgG+ cells. In sum, this study demonstrated distinct gene expression dynamics upon SARS-CoV-2 infection.

2020-12-11 | GSE161777 | GEO

Longitudinal multi-omics identifies responses of megakaryocytes, erythroid cells and plasmablasts as hallmarks of severe COVID-19 trajectories

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-12-11 | GSE161778 | GEO

Longitudinal Multi-omics Analyses Identify Responses of Megakaryocytes, Erythroid Cells, and Plasmablasts as Hallmarks of Severe COVID-19.

Project description: Not available

| S-EPMC7689306 | biostudies-literature

Longitudinal multi-omics identifies responses of megakaryocytes, erythroid cells and plasmablasts as hallmarks of severe COVID-19 trajectories [methylation]

Project description:To help characterise the temporal dynamics of host response during COVID-19, we performed a longitudinal DNA methylation analysis in a cohort of 12 patients. DNA was extracted from peripheral blood sampled at up to 5 time points per patient. At each sample point, a patient’s disease trajectory, “pseudotime”, was categorised according to clinical parameters. DNA methylation profiling by Illumina Bead Arrays was performed on each sample. We found CpG sites hypomethylated during COVID-19 were highly enriched in cis of transcripts related to positive regulation of TNF secretion and innate immune signalling, indicating potential long-term regulation of immunological misfiring by epigenetic processes.

2020-12-11 | GSE161678 | GEO

Longitudinal full-length IGH repertoire profiling and clonal lineage dynamics in memory B cells, plasmablasts and plasma cells of human peripheral blood

Project description:To study longitudinal dynamics of IGH BCR repertoires and clonal lineages evolution of memory B-cells, plasmablasts and plasma cells from peripheral blood of healthy donors, which were sampled three times within a year

2022-09-15 | E-MTAB-11193 | biostudies-arrayexpress

Gene expression profiles of cultured megakaryocytes

Project description:Cells obtained from adipose tissue are able to differentiate into megakaryocytes. We compared the gene expression profile of human adipose tissue derived megakaryocytes with that of megakaryocytes differentiated from human CD34 positive cord blood hematopoietic stem cells.

2021-04-05 | GSE112820 | GEO

CTCF binding in B cells and Plasmablasts

Project description:The mammalian CCCTC-binding factor (CTCF) regulates gene expression through the formation of higher order chromatin structures. Recent evidence has implicated a role for CTCF in regulating gene expression in the human MHCII locus. To investigate the role of CTCF in murine MHCII gene expression we mapped CTCF binding sites in B cells (MHCII+ cells) and Plasmablasts which are differentiated B cells that have silenced MHCII gene expression. These observations lead to the identification of differential CTCF binding during differentiation in these cell types and suggest mechanims of MHCII gene regulation. Comparison of CTCF binding in B cells and Plasmablasts in mice using ChIP-seq

2014-02-05 | E-GEOD-44637 | biostudies-arrayexpress

Relieving Dyrk1a repression of MKL1 corrects developmental defects in infantile megakaryocytes

Project description:Adult and fetal megakaryocytes are morphologically different. These differences contribute to neonatal thrombocytopenia in premature neonates and in neonates after infection and also contribute to poor megakaryocytes engraftment after umbilical cord blood transplant. We found that Dyrk1a kinase inhibition shift the fetal megakaryocytes phenotype toward adult phenotype. This effect is mediated by MKL1 the master regulator of megakaryocytes morphogenesis. To identify differences between adult and fetal megakaryocytes we performed RNA seq of adult derived megakaryocytes and fetal derived megakaryocytes treated and untreated with Dyrk inhibitors. Through this approach we identified cohorts of genes co-regulated in adult megakaryocytes and fetal megakaryocytes treated with the dyrk inhibitors. More importantly, we found that the dyrk inhibition in fetal megakaryocytes leads to upregulation of a significant number of MKL1 target genes.

2022-05-29 | GSE204909 | GEO

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