Unknown,Transcriptomics,Genomics,Proteomics

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Human Corneal Epithelial Cells (hTCEpi) 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 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).

ORGANISM(S): Homo sapiens

SUBMITTER: Cecilila Williams 

PROVIDER: E-GEOD-72662 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Vitamin D Induces Global Gene Transcription in Human Corneal Epithelial Cells: Implications for Corneal Inflammation.

Reins Rose Y RY   Mesmar Fahmi F   Williams Cecilia C   McDermott Alison M AM  

Investigative ophthalmology & visual science 20160501 6


<h4>Purpose</h4>Our previous studies show that human corneal epithelial cells (HCEC) have a functional vitamin D receptor (VDR) and respond to vitamin D by dampening TLR-induced inflammation. Here, we further examined the timing of the cytokine response to combined vitamin D-TLR treatment and used genome-wide microarray analysis to examine the effect of vitamin D on corneal gene expression.<h4>Methods</h4>Telomerase-immortalized HCEC (hTCEpi) were stimulated with polyinosinic-polycytidylic acid  ...[more]

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