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RNA-sequencing of human peripheral blood mononuclear cells (PB MNCs) and induced neural progenitor cells derived from PB MNCs

ABSTRACT: We have successfully generated human induced neural progenitor cells (iNPCs) from peripheral blood mononuclear cells (PB MNCs). To gain further insights into the transcriptional activation and cellular identity of human iNPCs, we compared the transcriptome of human iNPCs with PB MNCs and published database CORTECON and BrainSpan.

ORGANISM(S): Homo sapiens

PROVIDER: GSE107806 | GEO | 2019/11/21

REPOSITORIES: GEO

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RNA-sequencing of human peripheral blood mononuclear cells (PB MNCs) and induced neural progenitor cells derived from PB MNCs

Project description:RNA-sequencing of human peripheral blood mononuclear cells (PB MNCs) and induced neural progenitor cells derived from PB MNCs

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Direct generation of induced pluripotent stem cells from human non-mobilized blood

Project description:The use of induced pluripotent stem cells (iPSCs) is an exciting frontier in the study and treatment of human diseases through the generation of specific cell types. Here we show the derivation of iPSCs from human non-mobilized peripheral blood (PB) and bone marrow (BM) mononuclear cells (MNCs) by retroviral transduction of OCT3/4, SOX2, KLF4 and c-MYC. The PB- and BM-derived iPSCs were indistinguishable from human embryonic stem cells (hESCs) with respect to morphology, expression of surface antigens and pluripotency-associated transcription factors, global gene expression profiles and differentiation potential in vitro and in vivo. Infected PB and BM MNCs gave rise to iPSCs in the presence of several cytokines, although transduction efficiencies were not high. We found that 5×105 PB MNCs, which corresponds to less than 1 ml of PB, was enough for the generation of several iPSC colonies. Generation of iPSCs from MNCs of non-mobilized PB, with its relative efficiency and ease of harvesting, could enable the therapeutic use of patient-specific pluripotent stem cells.

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Gene expression signatures that predict radiation exposure (human)

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Gene expression signatures that predict radiation exposure (mouse)

Project description:Gene expression analysis of peripheral blood leukocytes (PB MNCs) to develop expression profiles that accurately reflect prior radiation exposure. Keywords: Comparative, exposure dosage, C57BI6 Murine Irradiation Studies We have made use of gene expression analysis of peripheral blood mononuclear cells (PB MNCs) to develop expression profiles that accurately reflect prior radiation exposure. Importantly, we demonstrate that expression profiles can be developed that not only predict radiation exposure in mice but also distinguish the level of radiation exposure, ranging from 50 cGy to 1000 cGy. Likewise, a molecular signature of radiation response developed solely from irradiated human patient samples can predict and distinguish irradiated human PB samples from non-irradiated samples with an accuracy of 90%, sensitivity of 85% and specificity of 94%. We further demonstrate that a radiation profile developed in the mouse can correctly distinguish PB samples from irradiated and non-irradiated human patients with an accuracy of 77%, sensitivity of 82% and specificity of 75%. Taken together, these data demonstrate that molecular profiles can be generated which are highly predictive of different levels of radiation exposure in mice and humans. Mouse Dataset only

2010-06-11 | E-GEOD-6873 | biostudies-arrayexpress

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RNA Microarray of 36H liver stages of Pb WT and Pb SSPELD Knock out parasites

Project description:Global gene expression profiling of P. berghei liver stages at 36h from WT and Pb SSPELD KO parasites to investigate the changes in RNA expression levels in Pb SSPELD parasites.

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IP of 5-methylcytosine (5-mc) enriched DNA fragments from control, PB treated mouse livers, resulting Ctnnb1 mutated PB liver tumours and PB minus Ha-Ras mutate liver tumour

Project description:Through the analysis of mouse liver tumours promoted by distinct routes (DEN exposure alone, DEN exposure plus non-genotoxic insult with phenobarbital and non-alcoholic fatty liver disease); we report that the cancer associated hyper-methylated CGI events in mice are also predicated by silent promoters that are enriched for both the DNA modification 5-hydroxymethylcytosine (5hmC) and the histone modification H3K27me3 in normal liver. During cancer progression these CGIs undergo hypo-hydroxymethylation, prior to subsequent hyper-methylation; whilst retaining H3K27me3. A similar loss of promoter-core 5hmC is observed in Tet1 deficient mouse livers indicating that reduced Tet1 binding at CGIs may be responsible for the epigenetic dysregulation observed during hepatocarcinogenesis. Consistent with this reduced Tet1 protein levels are observed in mouse liver tumour lesions. As in human, DNA methylation changes at CGIs do not appear to be direct drivers of hepatocellular carcinoma progression in mice. Instead dynamic changes in H3K27me3 promoter deposition are strongly associated with tumour-specific activation and repression of transcription. Our data suggests that loss of promoter associated 5hmC in diverse liver tumours licences DNA methylation reprogramming at silent CGIs during cancer progression. 5-mc is a well establisehd epigenetic mark typically related to gene silencing events. Phenobarbital (PB) is a well studied non-genotoxic carcinogen with roles in epigenetic perturbation. We profile 5mC in both control mouse livers as well as in the livers of 12 week PB treated mice. We also profile 5mC in liver tumours arising in the presence of long term PB exposure (35 week: resulting in Ctnnb1 mutated tumours) to a Ha-Ras liver tumour which arose without PB. Samples: 2 control and 2 PB exposed mouse livers, 3 liver tumours resulting from long term PB exposrue and 1 liver tumour arising without PB

2016-05-17 | E-GEOD-77727 | biostudies-arrayexpress

IP of 5-hydroxymethylcytosine (5-hmC) enriched DNA fragments from control ,PB treated mouse livers , resulting Ctnnb1 mutated PB liver tumours and PB minus Ha-Ras mutate liver tumour

Project description:Through the analysis of mouse liver tumours promoted by distinct routes (DEN exposure alone, DEN exposure plus non-genotoxic insult with phenobarbital and non-alcoholic fatty liver disease); we report that the cancer associated hyper-methylated CGI events in mice are also predicated by silent promoters that are enriched for both the DNA modification 5-hydroxymethylcytosine (5hmC) and the histone modification H3K27me3 in normal liver. During cancer progression these CGIs undergo hypo-hydroxymethylation, prior to subsequent hyper-methylation; whilst retaining H3K27me3. A similar loss of promoter-core 5hmC is observed in Tet1 deficient mouse livers indicating that reduced Tet1 binding at CGIs may be responsible for the epigenetic dysregulation observed during hepatocarcinogenesis. Consistent with this reduced Tet1 protein levels are observed in mouse liver tumour lesions. As in human, DNA methylation changes at CGIs do not appear to be direct drivers of hepatocellular carcinoma progression in mice. Instead dynamic changes in H3K27me3 promoter deposition are strongly associated with tumour-specific activation and repression of transcription. Our data suggests that loss of promoter associated 5hmC in diverse liver tumours licences DNA methylation reprogramming at silent CGIs during cancer progression. 5-hmC is a novel epigenetic mark derived from oxidation of methylcytosine. Phenobarbital (PB) is a well studied non-genotoxic carcinogen with roles in epigenetic perturbation. We profile 5hmC in both control mouse livers as well as in the livers of 12 week PB treated mice. We also profile 5hmC in liver tumours arising in the presence of long term PB exposure (35 week: resulting in Ctnnb1 mutated tumours) to a Ha-Ras liver tumour which arose without PB. Samples: 5hmC profiles in 2 control and 2 PB exposed mouse livers, 3 liver tumours resulting from long term PB exposrue and 1 liver tumour arising without PB

2016-05-17 | E-GEOD-77726 | biostudies-arrayexpress

PB enrichment culture

Project description:PB enrichment culture Raw sequence reads

| PRJNA774086 | ENA

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2014-12-11 | E-GEOD-64028 | biostudies-arrayexpress

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