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Links from GEO DataSets

Items: 10

1.

Comprehensive characterization of DNA methylation changes in Fuchs Endothelial Corneal Dystrophy

(Submitter supplied) Transparency of the human cornea is necessary for vision. Fuchs Endothelial Corneal Dystrophy (FECD) is a bilateral, heritable degeneration of the corneal endothelium, and a leading indication for corneal transplantation in developed countries. While the early onset, and rarer, form of FECD has been linked to COL8A2 mutations, the more common, late onset form of FECD has genetic mutations linked to only a minority of cases. more...
Organism:
Homo sapiens
Type:
Methylation profiling by genome tiling array
Platform:
GPL13534
16 Samples
Download data: IDAT, TXT
Series
Accession:
GSE94462
ID:
200094462
2.

Gene expression in Fuchs endothelial corneal dystrophy

(Submitter supplied) Fuchs’ endothelial corneal dystrophy (FECD) is a progressive vision impairing disease caused by thickening of Descemet’s membrane and gradual degeneration and loss of corneal endothelial cells. The aim of this study was to identify differentially expressed genes between FECD-affected and unaffected corneal endothelium to gain insight into the pathophysiological mechanisms underlying this disease. Microarray gene expression analysis was performed on total RNA from FECD-affected and unaffected corneal endothelium-Descemet’s membrane (CE-DM) specimens using the Illumina HumanHT-12 v3.0 expression array. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL10558
12 Samples
Download data: RDATA
Series
Accession:
GSE171830
ID:
200171830
3.

RNA Misplicing in Fuchs Endothelial Corneal Dystrophy II

(Submitter supplied) RNA-Seq splicing data from the corneal endothelia of FECD patients and controls reveal hundreds of differential alternative splicing events. These include events previously characterized in the context of myotonic dystrophy type 1 and epithelial-to-mesenchymal transition, as well as splicing changes in genes related to proposed mechanisms of FECD pathogenesis.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platforms:
GPL20301 GPL11154
28 Samples
Download data: TSV
4.

Epigenome analysis of normal human corneal endothelium and corneal endothelium from FECD patients

(Submitter supplied) Genome wide DNA methylation profiling of normal human corneal endothelium and human corneal endothelium from FECD cases. The Illumina Infinium MethylationEPIC 850K BeadChip was used to obtain DNA methylation profiles across approximately 850,000 CpGs in genomic DNA from human corneal endothelium samples. Samples included 11 non-FECD donors, 17 FECD cases.
Organism:
Homo sapiens
Type:
Methylation profiling by genome tiling array
Platform:
GPL21145
28 Samples
Download data: TXT
Series
Accession:
GSE198917
ID:
200198917
5.

Transcriptome Analysis of the Human Corneal Endothelium

(Submitter supplied) Defining the normal and age-dependent HCEnC transcriptome will further refine our understanding of the functional roles that the endothelium plays in the cornea and will provide a basis upon which to compare transcriptomes of normal and dystrophic endothelium for the subsequent development of gene-targeted therapies. We used microarrays to comprehensively characterize human corneal endothelial cell (HCEnC) gene expression, age-dependent differential gene expression and to identify expressed genes mapped to chromosomal loci associated with the corneal endothelial dystrophies PPCD1, FECD4 and XECD
Organism:
Homo sapiens
Type:
Expression profiling by array
Dataset:
GDS5432
Platform:
GPL11532
11 Samples
Download data: CEL
Series
Accession:
GSE58315
ID:
200058315
6.
Full record GDS5432

Age effect on corneal endothelium

Analysis of corneal endothelium from pediatric (4-11 years old) and adult (53-70 years old) donor corneas. Results provide insight into differential molecular expression between pediatric and adult corneal endothelial cells.
Organism:
Homo sapiens
Type:
Expression profiling by array, transformed count, 3 age sets
Platform:
GPL11532
Series:
GSE58315
9 Samples
Download data: CEL
7.

Serial analysis of gene expression in the corneal endothelium of Fuchs' dystrophy

(Submitter supplied) PURPOSE: To compare the gene expression profiles of normal human corneal endothelium with Fuchs' corneal endothelium, by using serial analysis of gene expression (SAGE). METHODS: Three pairs of normal human corneas were obtained from eye banks. Thirteen bisected Fuchs' corneal buttons were processed at the time of corneal transplantation. The endothelia of normal and Fuchs'-affected corneas were stripped, and total RNA was isolated. more...
Organism:
Homo sapiens
Type:
Expression profiling by SAGE
Platform:
GPL4
2 Samples
Download data
Series
Accession:
GSE505
ID:
200000505
8.

Start codon disruption with CRISPR/Cas9 prevents murine Fuchs' endothelial corneal dystrophy

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens; Mus musculus
Type:
Other
Platforms:
GPL24676 GPL16417
6 Samples
Download data: BW
Series
Accession:
GSE146999
ID:
200146999
9.

Indel rate analysis:Start codon disruption with CRISPR/Cas9 prevents murine Fuchs' endothelial corneal dystrophy

(Submitter supplied) A missense mutation of collagen type VIII alpha 2 chain (COL8A2) gene leads to early onset Fuchs’ endothelial corneal dystrophy (FECD), which can cause blindness through progressive loss of corneal endothelial cells. We established a novel procedure for achieving structural and functional rescue of the post-mitotic corneal endothelium without surgery, using CRISPR/Cas9-based postnatal gene editing in a mouse model of FECD. more...
Organism:
Mus musculus
Type:
Other
Platform:
GPL16417
4 Samples
Download data: XLSX
Series
Accession:
GSE146998
ID:
200146998
10.

Digenome for off-target analysis: Start codon disruption with CRISPR/Cas9 prevents murine Fuchs' endothelial corneal dystrophy

(Submitter supplied) A missense mutation of collagen type VIII alpha 2 chain (COL8A2) gene leads to early onset Fuchs’ endothelial corneal dystrophy (FECD), which can cause blindness through progressive loss of corneal endothelial cells. We established a novel procedure for achieving structural and functional rescue of the post-mitotic corneal endothelium without surgery, using CRISPR/Cas9-based postnatal gene editing in a mouse model of FECD. more...
Organism:
Homo sapiens
Type:
Other
Platform:
GPL24676
2 Samples
Download data: BW
Series
Accession:
GSE146997
ID:
200146997
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