Human Corneal Epithelial Cells (hTCEpi) 6h Treatment with 100nM Vitamin D (1,25D3) vs. Vehicle Control
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE72662 | GEO | 2016/09/01
SECONDARY ACCESSION(S): PRJNA294608
REPOSITORIES: GEO
Similar Datasets
Project description:Inflammatory signals must be regulated and kept in check in order to prevent tissue damage. This is especially true in the cornea, where damage can induce loss of transparency, essential for vision. Toll-like receptors (TLRs) are present at the ocular surface and, in addition to being protective against infection, have also been implicated in the pathogenesis of dry eye syndrome, an inflammatory condition that affects millions of individuals in the United States each year.  Therefore, an important area of research is the development of new anti-inflammatory therapeutics that limit aberrant ocular surface inflammation. Vitamin D has been studied for its role in suppressing inflammation in other tissues. In previous studies, we have demonstrated that vitamin D is able to decrease proinflammatory mediators induced by TLRs in human corneal epithelial cells (HCEC). Therefore, the goal of the current study was to examine this mechanism further through an evaluation of vitamin Dâ??s influence on gene expression in two different HCEC cell lines. Microarray comparing SV40-HCEC, human corneal epithelial cells, treated for 6 hours with Vitamin D (1,25D3) and control (0.1% ethanol) Two-condition arrays: SV40-HCEC cells were treated with either 100nM 1,25D3 or 0.1% Ethanol for 6h. Two biological replicates, one per array, with a dye swap (technical replicate).
2016-09-01 | E-GEOD-72663 | biostudies-arrayexpress
Project description:Inflammatory signals must be regulated and kept in check in order to prevent tissue damage. This is especially true in the cornea, where damage can induce loss of transparency, essential for vision. Toll-like receptors (TLRs) are present at the ocular surface and, in addition to being protective against infection, have also been implicated in the pathogenesis of dry eye syndrome, an inflammatory condition that affects millions of individuals in the United States each year. Therefore, an important area of research is the development of new anti-inflammatory therapeutics that limit aberrant ocular surface inflammation. Vitamin D has been studied for its role in suppressing inflammation in other tissues. In previous studies, we have demonstrated that vitamin D is able to decrease proinflammatory mediators induced by TLRs in human corneal epithelial cells (HCEC). Therefore, the goal of the current study was to examine this mechanism further through an evaluation of vitamin Dâs influence on gene expression in two different HCEC cell lines. Microarray comparing hTCEpi, human corneal epithelial cells, treated for 6 hours with Vitamin D (1,25D3) and control (0.1% ethanol) Two-condition arrays: hTCEpi cells were treated with either 100nM 1,25D3 or 0.1% Ethanol for 6h. Two biological replicates, one per array, with a dye swap (technical replicate).
2016-09-01 | E-GEOD-72662 | biostudies-arrayexpress
Project description:Inflammatory signals must be regulated and kept in check in order to prevent tissue damage. This is especially true in the cornea, where damage can induce loss of transparency, essential for vision. Toll-like receptors (TLRs) are present at the ocular surface and, in addition to being protective against infection, have also been implicated in the pathogenesis of dry eye syndrome, an inflammatory condition that affects millions of individuals in the United States each year. Therefore, an important area of research is the development of new anti-inflammatory therapeutics that limit aberrant ocular surface inflammation. Vitamin D has been studied for its role in suppressing inflammation in other tissues. In previous studies, we have demonstrated that vitamin D is able to decrease proinflammatory mediators induced by TLRs in human corneal epithelial cells (HCEC). Therefore, the goal of the current study was to examine this mechanism further through an evaluation of vitamin D’s influence on gene expression in two different HCEC cell lines. Microarray comparing SV40-HCEC, human corneal epithelial cells, treated for 6 hours with Vitamin D (1,25D3) and control (0.1% ethanol)
2016-09-01 | GSE72663 | GEO
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
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:Human Corneal Epithelial Cells (SV40-HCEC) 6h Treatment with 100nM Vitamin D (1,25D3) vs. Vehicle Control
| PRJNA294607 | ENA
Project description:Integrity of the cornea, the most anterior part of the eye is indispensable for vision. 45 million individuals are bilaterally blind and another 135 millions have severely impaired vision in both eyes because of loss of corneal transparency; treatments range from local medications to corneal transplants and more recently to stem cell therapy. The corneal epithelium is a squamous epithelium that is constantly renewing with a vertical turnover of seven to fourteen days in many mammals3. Identification of slow cycling cells (label-retaining cells or LRCs) in the limbus of the mouse has led to the notion that the limbus is the niche for the stem cells responsible for the long-term renewal of the cornea4; hence, the corneal epithelium is supposedly renewed by cells generated at and migrating from the limbus, in striking opposition to other squamous epithelia in which each resident stem cell has in charge a limited area of epithelium. Here, we show that the corneal epithelium of the mouse can be serially transplanted, is self-maintained and contains oligopotent stem cells with the capacity to generate goblet cells if provided with a conjunctival environment. In addition, the entire ocular surface of the pig, including the cornea, contains oligopotent stem cells (holoclones) with the capacity to generate individual colonies of corneal and conjunctival cells; hence, the limbus is not the only niche for corneal stem cells and corneal renewal is not different from other squamous epithelia. Experiment Overall Design: Expression profile difference between keratinocyte clones from conjunctiva and cornea (3 individual clones in each group)
2008-10-25 | E-GEOD-12604 | biostudies-arrayexpress
Project description:The cornea is the transparent tissue covering the anterior part of the eye. Its main roles are to convey the light toward the retina, and to act as a protective barrier against infection or injury for the eye. The transparency of the cornea is a crucial component of its functionality and is the result of specific architecture and cell arrangements. The inner layer of the cornea is the endothelium, composed of a monolayer of endothelial cells. The next layer is the stroma, representing about two third of the thickness of the cornea, and is mainly composed of a specifically arranged extracellular matrix, secreted by few keratocytes1–4. Finally, the external layer is a life-long renewed pluristratified epithelium. The regulated epithelial homeostasis, crucial to maintain the corneal transparency, relies on stem and progenitor cells5. To coordinate epithelial homeostasis and healing, and to adequately respond to any change in the corneal environment, this tissue is highly innervated6,7. The corneal innervation is mainly composed of A and C sensory fibres whose cell bodies are located in the ophthalmic branch of the trigeminal ganglion8. Those fibres penetrate the corneal stroma from the periphery, as bundles of fibres branching and spreading within the stroma9. When entering in the epithelium, the fibres branche again and radiate horizontally to form the subbasal plexus. Finally, the sensory fibres shift orientation to reach the top of the epithelium, where they end up as free nerve endings6,7. There are three classes of fibres innervating the cornea: the mechano-nociceptors, the cold sensing neurons and the polymodal nociceptors, reacting respectively to mechanical, thermal and chemical stimuli10,11. Stimuli transduction is not the only role of the corneal innervation, as these fibres have a crucial role on epithelial homeostasis through the secretion of trophic factors essential for epithelial cell survival12. Due to its localization, the cornea is highly exposed to ultraviolet radiation and high oxygen tension, making it particularly vulnerable to mitochondrial defects13. These defects can be either inherited or non-inherited. Inherited forms result from mutations in mitochondrial DNA (mtDNA) or nuclear gene defects affecting mitochondrial function14. Inherited mitochondrial dysfunction is a key factor in the progression of Fuchs endothelial corneal dystrophy (FECD) and keratoconus13,15,16. Non-inherited mitochondrial dysfunction, on the other hand, can occur due to spontaneous mtDNA mutations or somatic mutations that accumulate with age, rendering the mitochondrial metabolism less efficient with time17. To date, the impact of inherited mitochondrial dysfunctions on corneal epithelium physiology has not been extensively studied. Case reports have linked mitochondrial diseases to corneal cloudiness18,19, perforation20 and edema21. Furthermore, mitochondrial defect was associated to inflammatory context and ROS production in ocular surface pathologies13,22. Despite these studies, the direct effect of mitochondrial disfunction on corneal biology remains elusive. Among the known pathologies originating from an inherited mitochondrial dysfunction, the dominant optic atrophy (DOA) is an inherited blinding disease caused by the degenescence of the retinal cell ganglions forming the optic nerve23. The mutation of the gene OPA1 is responsible for the majority of the DOA diagnostics. OPA1 gene encodes for a mitochondrial protein involved in the fusion process and is essential to maintain the organelle integrity. Generally, optic neuropathy is the characteristic syndrome for DOA, but a subset of patients, called dominant optic atrophy plus (DOA+), also declare extra-ocular syndromes such as ataxia, deafness and peripheral neuropathies24,25. A mouse model, bearing the OPA1delTTAG mutation, recapitulates the degenerative syndromes encountered in DOA+ patients25.. While DOA is associated with lens cloudiness, no report has linked DOA to ocular surface defects. Here, we investigated the impact of OPA1 delTTAG mutation on mouse cornea as its structure includes a large amout of sensory fibres that are crucial to maintain corneal homeostasis.
2024-07-25 | PXD052337 | Pride
Project description:Integrity of the cornea, the most anterior part of the eye is indispensable for vision. 45 million individuals are bilaterally blind and another 135 millions have severely impaired vision in both eyes because of loss of corneal transparency; treatments range from local medications to corneal transplants and more recently to stem cell therapy. The corneal epithelium is a squamous epithelium that is constantly renewing with a vertical turnover of seven to fourteen days in many mammals3. Identification of slow cycling cells (label-retaining cells or LRCs) in the limbus of the mouse has led to the notion that the limbus is the niche for the stem cells responsible for the long-term renewal of the cornea4; hence, the corneal epithelium is supposedly renewed by cells generated at and migrating from the limbus, in striking opposition to other squamous epithelia in which each resident stem cell has in charge a limited area of epithelium. Here, we show that the corneal epithelium of the mouse can be serially transplanted, is self-maintained and contains oligopotent stem cells with the capacity to generate goblet cells if provided with a conjunctival environment. In addition, the entire ocular surface of the pig, including the cornea, contains oligopotent stem cells (holoclones) with the capacity to generate individual colonies of corneal and conjunctival cells; hence, the limbus is not the only niche for corneal stem cells and corneal renewal is not different from other squamous epithelia. Keywords: Cell type comparison
2008-08-29 | GSE12604 | GEO
Project description:We successfully induced corneal epithelial cells from human iPSCs. Then, we perfomed global expression analysis using microarray to compare the character of hiPSC-derived corneal epithelial cells with that of the other kinds of cells. Total RNA was obtained from human iPSCs (hiPSCs), human iPSC-derived corneal epithelial cells (hiCECs), human corneal limbal epithelial cells (HCECs), human oral keratinocytes (HOKs), human dermal fibroblasts (HDFs) and six weeks-differentiated hiPSCs (hiPSC-derived ocular surface ectoderm, OSE) using the QIAZol reagent. A microarray analysis using Sure Print G3 human 8x60K slides (Agilent technologies) was performed at Takara Bio (Shiga, Japan).
2016-03-09 | E-GEOD-73971 | biostudies-arrayexpress