Abstract

Abstract Purpose The meibomian gland is extremely important in maintaining the health and integrity of the ocular surface. This gland, through its lipid synthesis and secretion, promotes the stability and prevents the evaporation of the tear film. Conversely, meibomian gland dysfunction (MGD) leads to a decreased stability and increased evaporation of the tear film. Indeed, meibomian gland dysfunction is thought to be the major cause of dry eye syndromes throughout the world. Our goal is to advance understanding of the regulation of meibomian gland function and the mechanisms underlying MGD. Methods Procedures included the immortalization of human meibomian gland epithelial cells with human telomerase reverse transcriptase, the evaluation of cellular responsiveness, and the identification of glandular gene expression changes in MGD. Gene analyses were conducted with Illumina HumanHT‐12 v3 Expression BeadChips and Geospiza bioinformatics software. Results To date we have [a] immortalized human meibomian gland epithelial cells that respond to secretagogue, growth factor, neurotransmitter and hormone exposure with alterations in proliferation, differentiation, signaling, gene expression and/or lipogenesis; [b] discovered human meibomian gland genes that may facilitate the development and/or progression of MGD. These genes encode proteins that promote keratinization and amplify inflammation. Conclusion Our findings advance our understanding of the control of the meibomian gland in both health and disease. [Acknowledgments: S.M. Richards, M. Hatton, A.M. Fay and K. Lo; Supported by grants from NIH (R01EY05612) and Alcon] Commercial interest

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