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

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).