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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Molecular Signatures of cardiac defects in Down syndrome lymphoblastoid cell lines (trisomy 21)

ABSTRACT: Molecular consequences of trisomy in lymphoblastoid cell lines from patients with Down syndrome. This project analyses differentially expressed genes between humans with trisomy 21 and humans without trisomy 21. Total RNA obtained from human lymphoblastoid cell lines without trisomy 21 compared to cell lines from human with trisomy 21.

ORGANISM(S): Homo sapiens

SUBMITTER: Luce Dauphinot

PROVIDER: E-GEOD-34458 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Molecular Signatures of cardiac defects in Down syndrome lymphoblastoid cell lines (trisomy 21)

Project description:Molecular consequences of trisomy in lymphoblastoid cell lines from patients with Down syndrome. This project analyses differentially expressed genes between humans with trisomy 21 and humans without trisomy 21.

2012-08-15 | GSE34458 | GEO

Molecular Signatures of cardiac defects in Down syndrome lymphoblastoid cell lines (congenital heart disease)

Project description:Molecular Signatures of cardiac defects in Down syndrome lymphoblastoid cell lines. In this study, we want to identify genes and pathways specifically dysregulated in atrioventricular septal defect and /or atrial septal defect + ventricular septal defect in case of trisomy 21. Total RNA obtained from DS lymphoblastoid cell lines without congenital heart disease compared to cell lines from DS with congenital heart disease.

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Molecular Signatures of cardiac defects in Down syndrome lymphoblastoid cell lines

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Trisomy 21 and TS13

Project description:Gene expression was measured in trisomy 21 and trisomy 13 human fetal samples. For TS21, regions assayed were cerebrum, cerebellum, heart, and cerebrum-derived astrocyte cell lines. Keywords = trisomy 21 Keywords = Down syndrome Keywords = aneuploidy Keywords = brain Keywords = heart Keywords = trisomy 13 Keywords: other

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RNA-seq of human aneuploid cell lines with Trisomy 21

Project description:Trisomy 21, a form of aneuploidy, is one of the few viable forms of trisomy. The goal of this study was to assess the effect of an additional chromosome 21 on gene expression in two different human aneuploid model cell lines.

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Transcription profiling of human fetal cerebellum, heart, cerebrum, and cerebrum derived astrocyte cell line from trisomy 21 and trisomy 13 samples

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Transcriptional Consequences of Trisomy 21 on Neural Induction

Project description:Down syndrome, caused by trisomy 21, is a complex developmental disorder associated with intellectual disability and reduced growth of multiple organs. Structural pathologies are present at birth, reflecting embryonic origins. A fundamental unanswered question is how an extra copy of human chromosome 21 contributes to organ-specific pathologies that characterize individuals with Down syndrome. Relevant to the hallmark intellectual disability in Down syndrome, how does trisomy 21 affect neural development? We tested the hypothesis that trisomy 21 exerts effects on human neural development as early as neural induction. Bulk RNA sequencing was performed on isogenic trisomy 21 and euploid human induced pluripotent stem cells (iPSCs) at successive stages of neural induction: embryoid bodies at Day 6, early neuroectoderm at Day 10, and differentiated neuroectoderm at Day 17. Gene expression analysis revealed over 1,300 differentially expressed genes in trisomy 21 cells along the differentiation pathway compared to euploid controls. Less than 5% of the gene expression changes included upregulated chromosome 21 encoded genes at every timepoint. Genes involved in specific growth factor signaling pathways (Wnt and Notch), metabolism (including interferon response and oxidative stress), and extracellular matrix were altered in trisomy 21 cells. Further analysis revealed heterochronic expression of genes. This comprehensive analysis reveals that trisomy 21 impacts discrete developmental pathways at the earliest stages of neural development. Further, the results suggest that metabolic dysfunction arises early in embryogenesis in trisomy 21 and may thus affect development and function more broadly.

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