Transcriptome of Immortalized Mouse Corneal Endothelial Cells with SLC4A11 deficiency
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA597783 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10769300.fastq.gz | Fastqsanger.gz | |||
| SRR10769301.fastq.gz | Fastqsanger.gz | |||
| SRR10769302.fastq.gz | Fastqsanger.gz | |||
| SRR10769303.fastq.gz | Fastqsanger.gz | |||
| SRR10769304.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 12 |
Similar Datasets
Project description:Mutations in the solute-linked carrier family 4 member 11 (SLC4A11) gene are associated with several corneal endothelial dystrophies, in all of which visually significant cornea edema may require corneal transplantation. To elucidate the pathogenesis of SLC4A11 associated corneal endothelial dystrophies, we analyzed the transcriptome of immortalized mouse corneal endothelial cells (Slc4a11-/- MCEnC) and Slc4a11+/+ MCEnC as controls.
2020-08-13 | GSE142635 | GEO
Project description:Mutations in the solute-linked carrier family 4 member 11 (SLC4A11) gene are associated with several corneal endothelial dystrophies, in all of which visually significant cornea edema may require corneal transplantation. To elucidate the pathogenesis of SLC4A11 associated corneal endothelial dystrophies, we analyzed the transcriptome of SLC4A11 knock-down primary human corneal endothelium (SLC4A11 KD pHCEnC) and scrambled RNA treated pHCEnC as controls.
2020-08-13 | GSE142636 | GEO
Project description:Transcriptome of Human Primary Corneal Endothelial Cells with SLC4A11 deficiency
| PRJNA597782 | ENA
Project description:The corneal endothelium plays a primary role in maintaining corneal homeostasis and clarity, and must be surgically replaced with allogenic donor corneal endothelium in the event of visually significant dysfunction. However, a worldwide shortage of donor corneal tissue has led to a search for alternative sources of transplantable tissue. Cultured human corneal endothelial cells (HCEnC) have been shown to restore corneal clarity in experimental models of corneal endothelial dysfunction in animal models, but characterization of cultured HCEnC remains incomplete. To this end, we utilized next-generation RNA sequencing technology to compare the transcriptomic profile of ex vivo human corneal endothelium (evHCEnC) with that of primary HCEnC and HCEnC lines, and to determine the utility of cultured and immortalized corneal endothelial cells as models of in vivo corneal endothelium. Multidimensional analyses of the transcriptome datasets demonstrated that primary HCEnC have a closer relationship to evHCEnC than do immortalized HCEnC. Subsequent analyses showed that the majority of the genes specifically expressed in HCEnC (not expressed in ex vivo corneal epithelium or fibroblasts) demonstrated a marked variability of expression in cultured cells compared with evHCEnC. In addition, genes associated with either corneal endothelial cell function or corneal endothelial dystrophies were investigated. Significant differences in gene expression and protein levels were observed in the cultured cells compared with evHCEnC for each of the genes tested except for AGBL1 and LOXHD1, which were not detected by RNA-seq or qPCR. Our transcriptomic analysis suggests that at a molecular level primary HCEnC most closely resemble evHCEC and thus represent a viable therapeutic option for managing corneal endothelial dysfunction. Our findings also suggest that investigators should perform an assessment of the entire transcriptome of cultured HCEnC prior to determination of the potential clinical utility of the cultured HCEnC for the management of corneal endothelial cell failure. Transcriptomes from ex vivo corneal endothelium, primary cultures and three cell lines were compared. Three samples of each endothelial cell group were submitted for RNA sequencing for a total of 15 samples. The transcriptome for the ex vivo corneal endothelium was used as the reference (i.e., proxy for in vivo corneal endothelium). Transcript abundances for a subset of genes associated with corneal endothelial cell function or disease were validated with qPCR and western blot. Samples of ex vivo endothelium used for validation were independent replicates not used for RNA-sequencing.
2015-09-04 | E-GEOD-65991 | biostudies-arrayexpress
Project description:Human corneal endothelial cells (HCEC) form a monolayer by adhering tightly through their intercellular adhesion molecules. Located at the posterior corneal surface, they maintain corneal translucency by dehydrating the corneal stroma, mainly through the Na+- and K+-dependent ATPase (Na+/K+-ATPase). Because HCEC proliferative activity is low in vivo,we tried to activate proliferation of HCEC by inhibiting cyclin-dependent kinase inhibitors.We have here demonstrated microarray data of transduced human corneal endothelial cell lines. Affymetrix human U133 plus 2.0 array was used to transcriptionally profile to compare cultured human corneal endothelial cells and transduced human corneal endothelial cells.
2011-10-29 | E-GEOD-30781 | biostudies-arrayexpress
Project description:The corneal endothelium plays a primary role in maintaining corneal homeostasis and clarity, and must be surgically replaced with allogenic donor corneal endothelium in the event of visually significant dysfunction. However, a worldwide shortage of donor corneal tissue has led to a search for alternative sources of transplantable tissue. Cultured human corneal endothelial cells (HCEnC) have been shown to restore corneal clarity in experimental models of corneal endothelial dysfunction in animal models, but characterization of cultured HCEnC remains incomplete. To this end, we utilized next-generation RNA sequencing technology to compare the transcriptomic profile of ex vivo human corneal endothelium (evHCEnC) with that of primary HCEnC and HCEnC lines, and to determine the utility of cultured and immortalized corneal endothelial cells as models of in vivo corneal endothelium. Multidimensional analyses of the transcriptome datasets demonstrated that primary HCEnC have a closer relationship to evHCEnC than do immortalized HCEnC. Subsequent analyses showed that the majority of the genes specifically expressed in HCEnC (not expressed in ex vivo corneal epithelium or fibroblasts) demonstrated a marked variability of expression in cultured cells compared with evHCEnC. In addition, genes associated with either corneal endothelial cell function or corneal endothelial dystrophies were investigated. Significant differences in gene expression and protein levels were observed in the cultured cells compared with evHCEnC for each of the genes tested except for AGBL1 and LOXHD1, which were not detected by RNA-seq or qPCR. Our transcriptomic analysis suggests that at a molecular level primary HCEnC most closely resemble evHCEC and thus represent a viable therapeutic option for managing corneal endothelial dysfunction. Our findings also suggest that investigators should perform an assessment of the entire transcriptome of cultured HCEnC prior to determination of the potential clinical utility of the cultured HCEnC for the management of corneal endothelial cell failure.
2015-09-04 | GSE65991 | GEO
Project description:Genome-wide analysis of dihydrotestosterone (DHT) induced changes in gene expression in primary and immortalized human corneal epithelial cells. Analysis of regulation of primary and immortalized human corneal epithelial cells by dihydrotestosterone at gene expression level. The hypothesis tested in the present study was that the androgen-eye interaction in ocular surface epithelial cells like corneal cells is influenced by androgens through regulation of the expression of multiple genes. Results provide important information of the differential regulation and comparitive analysis of numerous genes in response to dihydrotestosterone incubation in primary and immortalized human corneal epithelial cells. Total RNA was obtained from primary and immortalized human corneal epithelial cells treated for 5 days with 10 nM dihydrotestosterone (n=3) or vehicle (n=3). The RNA was then used with Illumina HumanHT-12 v3 Expression BeadChips to determine the effect of DHT on gene expression in the primary human corneal cells grown in our laboratory and the immortalized human corneal epithelial cell line developed in Dr. Rheinwald's laboratory [Rheinwald et al. MCB, 22 (14): 5157. (2002)] and charecterized in Dr. Ilene Gibson's laboratory [Gipson et al. IOVS, 44 (6): 2496. (2003)].
2011-03-31 | E-GEOD-18093 | biostudies-arrayexpress
Project description:Genome-wide analysis of dihydrotestosterone (DHT) induced changes in gene expression in primary and immortalized human corneal epithelial cells. Analysis of regulation of primary and immortalized human corneal epithelial cells by dihydrotestosterone at gene expression level. The hypothesis tested in the present study was that the androgen-eye interaction in ocular surface epithelial cells like corneal cells is influenced by androgens through regulation of the expression of multiple genes. Results provide important information of the differential regulation and comparitive analysis of numerous genes in response to dihydrotestosterone incubation in primary and immortalized human corneal epithelial cells.
2011-03-31 | GSE18093 | GEO
Project description:This dataset contains proteomic profiles of Descemet's membrane (DM) with corneal endothelial cells derived from patients with Fuchs endothelial corneal dystrophy (FECD) and non-FECD subjects by shotgun proteomics. FECD is the most common inherited corneal disease. Fibrillar focal excrescences, called guttae, and corneal edema due to corneal endothelial cell death result in progressive vision loss. Our dataset indicated that 32 distinctive molecules were expressed only in the FECD-DM but not in the DM of the control subject, possibly having important roles in the pathophysiology of FECD.
2023-01-17 | MSV000091078 | MassIVE
Project description:Human corneal endothelial cells (HCEC) form a monolayer by adhering tightly through their intercellular adhesion molecules. Located at the posterior corneal surface, they maintain corneal translucency by dehydrating the corneal stroma, mainly through the Na+- and K+-dependent ATPase (Na+/K+-ATPase). Because HCEC proliferative activity is low in vivo,we tried to activate proliferation of HCEC by inhibiting cyclin-dependent kinase inhibitors.We have here demonstrated microarray data of transduced human corneal endothelial cell lines.
2011-10-30 | GSE30781 | GEO