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RNA-sequencing of brain microvascular endothelial cell dysfunction in an isogenic juvenile iPSC model of Huntington’s disease

ABSTRACT: RNA-sequencing of brain microvascular endothelial cell dysfunction in an isogenic juvenile iPSC model of Huntington’s disease

PROVIDER: PRJNA800452 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17745603_1.fastq.gz	Fastqsanger.gz
	SRR17745603_2.fastq.gz	Fastqsanger.gz
	SRR17745604_1.fastq.gz	Fastqsanger.gz
	SRR17745604_2.fastq.gz	Fastqsanger.gz
	SRR17745605_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

RNA-sequencing of brain microvascular endothelial cell dysfunction in an isogenic juvenile iPSC model of Huntington’s disease

Project description:Huntington's disease (HD) is associated with dysfunction of the blood-brain barrier, including brain microvasscular endothelial cells (BMECs). We report changes in gene expression of induced pluripotent stem cells (iPSCs) and iPSC-derived brain microvascular endothelial cell-like cells (iBMECs) derived from an isogenic pair of iPSCs with either 180 (HD-corrected) or 18 (HD180) CAG repeats in the HTT gene.

2022-02-01 | GSE194416 | GEO

mRNAseq of Huntington's disease and control patient iPSC-derived brain microvascular endothelial cells

Project description:Purpose: The goals of this study are to compare the transcriptomic profile (mRNA-seq) of HD and control patient iPSC-derived brain microvascular endotheial cells to identify alterations in gene expression. Methods: RNA were isolated from HD and control iPSC-derived brain microvascular endothelial cells. mRNAseq using Illumina TruSeq mRNA PolyA+ v2 lib prep and HiSeq 2500. Statistical difference in mRNA levels were calculated with subsequent GO and pathway analysis. Results: mRNAseq and statistical analysis revealed differentially expressed genes between HD and control iPSC-derived brain microvascular endothelial cells. Conclusions: Our study shows differentially expressed genes between HD and control iPSC-derived brain microvascular endothelial cells, and reveals gene networks that are relevant to the mechanism of HD pathogenesis.

2017-05-16 | GSE97100 | GEO

Brain microvascular endothelial cell dysfunction in an isogenic juvenile iPSC model of Huntington's disease.

Project description:Huntington's disease (HD) is an inherited neurodegenerative disease caused by expansion of cytosine-adenine-guanine (CAG) repeats in the huntingtin gene, which leads to neuronal loss and decline in cognitive and motor function. Increasing evidence suggests that blood-brain barrier (BBB) dysfunction may contribute to progression of the disease. Studies in animal models, in vitro models, and post-mortem tissue find that disease progression is associated with increased microvascular density, altered cerebral blood flow, and loss of paracellular and transcellular barrier function. Here, we report on changes in BBB phenotype due to expansion of CAG repeats using an isogenic pair of induced pluripotent stem cells (iPSCs) differentiated into brain microvascular endothelial-like cells (iBMECs). We show that CAG expansion associated with juvenile HD alters the trajectory of iBMEC differentiation, producing cells with ~ two-fold lower percentage of adherent endothelial cells. CAG expansion is associated with diminished transendothelial electrical resistance and reduced tight junction protein expression, but no significant changes in paracellular permeability. While mutant huntingtin protein (mHTT) aggregates were not observed in HD iBMECs, widespread transcriptional dysregulation was observed in iBMECs compared to iPSCs. In addition, CAG expansion in iBMECs results in distinct responses to pathological and therapeutic perturbations including angiogenic factors, oxidative stress, and osmotic stress. In a tissue-engineered BBB model, iBMECs show subtle changes in phenotype, including differences in cell turnover and immune cell adhesion. Our results further support that CAG expansion in BMECs contributes to BBB dysfunction during HD.

| S-EPMC9245306 | biostudies-literature

RNA-seq analysis of iPSC-derived brain microvascular endothelial cells following long-term cryopreservation

Project description:We report changes in gene expression from iPSC to iPSC-derived brain microvascular endothelial cells (dhBMECs) and from one-year cryopreservation of dhBMECs.

2020-06-08 | GSE151976 | GEO

SARS-CoV-2 causes dysfunction in human iPSC-derived brain microvascular endothelial like cells potentially by signal modulation

Project description:SARS-CoV-2 is considered to affect the central nervous system (CNS) by interacting with the blood–brain barrier (BBB), which is defined by tight junctions that seal paracellular gaps between brain microvascular endothelial like cells (BMECs). Although SARS-CoV-2 infection of BMECs has been reported, the mechanism has not been fully elucidated. Here, we investigated the mechanism using iPSC derived brain microvascular endothelial like cells (iPSC-BMELCs). We observed that iPSC-BMELCs were infected with SARS-CoV-2, which resulted in inflammatory responses. RNA-seq analysis revealed that SARS-CoV-2 modulated the expression of signal molecules in iPSC-BMELCs. These findings suggest that SARS-CoV-2 infection causes BBB dysfunction in humans.

2024-02-01 | GSE254309 | GEO

WGS of KCNQ2 R201C patient derived iPSC and its isogenic line

Project description:Using prime editing, we generated an isogenic line of an iPSC line of an individual with a pathogenic KCNQ2 R201C mutation. WGS on the mutant line and two isogenic clones was performed to identify potential off target effects

| EGAS00001007231 | EGA

RNA-seq expression data from Human iPSC-derived Brain Microvascular Endothelial-like Cells (iBMECs)

Project description:Comparison of Human iPSC-derived Brain Microvascular Endothelial-like Cells (iBMECs) grown in poly(dimethylsiloxane) tissue chips. Data contains RNA-seq profiles of iBMECs exposed to various levels of shear stress ranging from 0, 0.01, 0.5, and 2.4 dyn/cm2; as well as RNA-seq profiles of FACS sorted iBMECs cultured alone or with primary human astrocytes and pericytes or with iPSC-derived neural progenitor cells.

2019-06-05 | GSE129290 | GEO

Transcriptional Profiling of Werner Syndrome (WS) iPSC-derived MSC and the isogenic gene-edited controls

Project description:WS iPSC (iWS780) is a WRN-null iPSC line derived from AG00780 fibroblast. This iPSC line showed normal 46,XY karyotype. iWS780 was gene-edited by CRIPSR/Cas9 to correct the WRN point mutation. Two clones (C21 & C24) were characterized and showed expression of wild-type WRN protein after gene editing. The iPSC lines (isogenic) were subsequently differentiated into mesenchymal stem cells (MSC). RNA-seq was performed on these MSC.

2019-09-24 | GSE137856 | GEO

RNA sequencing of human iPSC-derived brain microvascular endothelial cells.

Project description:RNA sequencing of human iPSC-derived brain microvascular endothelial cells.

| PRJEB36836 | ENA

Transcript abundance in A-T-derived iPSC: Comparing isogenic cells to unrelated individual

Project description:Induced pluripotent stem cells (iPSC) were prepared from multiple subjects with Ataxia-telangiectasia (A-T). iPSC were prepared from activated T-cells using commercial Sendai virus to deliver reprogramming factors. ATM protein-expressing and non-expressing cultures would found in multiple sub-lines (sub-lines are generated from distinct founder colonies of cells) from a single subject (Q3). Genetic analysis determined that all sub-lines originated from the same subject and were likely the product of spontaneous reversion by gene correction. To compare gene expression profiles, three iPSC samples were assayed: (1) A reverted ATM+/- subline from subject Q3, (2) An ATM-/- subline from subject Q3, and (3) An iPSC line from an unrelated ATM-/- subject, Q1. Analysis reveals that the majority of significantly-different genes between the unrelated ATM-/- line (Q1SA) and the reverted ATM+/- line (Q3SC) was due to genetic variation between individuals. A more focused set of contrasting genes could be identified between the isogenic Q3-derived lines (Q3SA, ATM-/-, vs. Q3SC, ATM+/-). The 206 transcripts that are significantly different point to a differential regulation of p53-associated pathways. Total cellular RNA was prepared from each iPSC culture. Different passage numbers or sister cultures were used as replicates (n=2).

2015-11-19 | E-GEOD-71878 | biostudies-arrayexpress

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