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Human Corneal Epithelial Cells (SV40-HCEC) 6h Treatment with 100nM Vitamin D (1,25D3) vs. Vehicle Control

ABSTRACT: 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)

ORGANISM(S): Homo sapiens

PROVIDER: GSE72663 | GEO | 2016/09/01

SECONDARY ACCESSION(S): PRJNA294607

REPOSITORIES: GEO

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Human Corneal Epithelial Cells (SV40-HCEC) 6h Treatment with 100nM Vitamin D (1,25D3) vs. Vehicle Control

Project description:Inflammatory signals must be regulated and kept in check in order to prevent tissue damage.Â This is especially true in the cornea, where damage can induce loss of transparency, essential for vision.Â 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.Â Â Therefore, an important area of research is the development of new anti-inflammatory therapeutics that limit aberrant ocular surface inflammation.Â Vitamin D has been studied for its role in suppressing inflammation in other tissues.Â In previous studies, we have demonstrated that vitamin D is able to decrease proinflammatory mediators induced by TLRs in human corneal epithelial cells (HCEC).Â 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

Human Corneal Epithelial Cells (hTCEpi) 6h Treatment with 100nM Vitamin D (1,25D3) vs. Vehicle Control

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

Human Corneal Epithelial Cells (hTCEpi) 6h Treatment with 100nM Vitamin D (1,25D3) vs. Vehicle Control

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 hTCEpi, human corneal epithelial cells, treated for 6 hours with Vitamin D (1,25D3) and control (0.1% ethanol)

2016-09-01 | GSE72662 | GEO

Expression data from human corneal endothelial cells

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

Expression data from human corneal endothelial cells

2011-10-29 | E-GEOD-30781 | biostudies-arrayexpress

Transcriptomic analysis of APC knock down HCEC 1CT cells compared to the wild type HCEC 1CT cells.

Project description:We performed RNA sequencing analysis of two human colon epithelial cell lines (HCEC 1CT_WT and HCEC 1CT_APC KD).

2020-09-25 | GSE152562 | GEO

APC knock down HCEC 1CT cells compared to the wild type HCEC 1CT cells

Project description:APC knock down HCEC 1CT cells compared to the wild type HCEC 1CT cells

| PRJNA640310 | ENA

Expression data from human iPSC-derived corneal epithelial cells

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

Single cell transcriptomic analysis of APC knockdown in HCEC 1CT cells.

Project description:In order to investigate sophisticated events during cancer initiation, we established early colorectal cancer development model. We performed scRNA-seq and analyzed the scRNA-seq dataset. scRNA-seq was conducted at 3- and 7-days after transduction of shRNA targeting APC (shAPC) and scrambled shRNA (shScr) on HCEC 1CT cells.

2020-09-25 | GSE152745 | GEO

Gene expression profile of human monocytes stimulated with all-trans retinoic acid (ATRA) or 1,25a-dihydroxyvitamin D3 (1,25D3)

Project description:A role for vitamin A in host defense against Mycobacterium tuberculosis has been suggested through epidemiological and in vitro studies; however, the antimicrobial mechanism is unclear. Here, we demonstrate that vitamin A mediates host defense through regulation of cellular cholesterol content. Comparison of monocytes stimulated with all-trans retinoic acid (ATRA) or 1,25-dihydroxyvitamin D3, the biologically active forms of vitamin A and vitamin D respectively, indicates that ATRA and 1,25D3 induce mechanistically distinct antimicrobial activities. Gene expression profiling reveals that ATRA but not 1,25D3 triggers a lipid metabolism and efflux pathway, including expression of lysosomal lipid transport gene NPC2. ATRA-induced decrease in total cellular cholesterol content, subcellular lipid reorganization, lysosomal acidification and antimicrobial activity are all dependent upon expression of NPC2. Finally, the addition of HIV-protease inhibitors known to inhibit cholesterol efflux, Ritonavir and Nelfinavir, blocked both ATRA-induced cholesterol decrease as well as antimicrobial activity. Taken together, these results suggest that the vitamin A-mediated host defense mechanism against M. tuberculosis requires regulation of cellular cholesterol. Monocytes derived from four independent healthy blood donors that were stimulated with control (CTRL), ATRA or 1,25D3 at 10-8M for 18 hours.

2013-12-31 | E-GEOD-46268 | biostudies-arrayexpress

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