Meibomian gland dysfunction (MGD) may be the leading cause of dry eye syndrome throughout the world. However, the precise mechanism(s) underlying the pathogenesis of this disease is unclear. We sought to identify meibomian gland genes that may promote the development and/or progression of human MGD.
Lid tissues were obtained from male and female MGD patients and age-matched controls after eyelid surgeries (e.g. to correct entropion or ectropion). Meibomian glands were isolated and processed for RNA extraction and the analysis of gene expression using BeadChips.
Our results show that MGD is associated with significant alterations in the expression of almost 400 genes in the human meibomian gland. The levels of 197 transcripts, including those encoding various small proline-rich proteins and S100 calcium binding proteins, are significantly increased, while the expression of 194 genes, such as for claudin 3 and cell adhesion molecule 1, is significantly decreased. These changes, which cannot be accounted for by sex differences, are accompanied by alterations in many gene ontologies (e.g. keratinization, cell cycle and DNA repair). Our findings also show that the human meibomian gland contains a number of highly expressed genes that are distinct from those in an adjacent tissue (i.e. conjunctival epithelium).
Our results demonstrate that MGD is accompanied by multiple changes in gene expression in the meibomian gland. The nature of these alterations, including the upregulation of genes encoding small proline-rich proteins and S100 calcium binding proteins, suggest that keratinization plays an important role in the pathogenesis of MGD.
Invest Ophthalmol Vis Sci. 2011 Mar 2. [Epub ahead of print]
Liu S, Richards SM, Lo K, Hatton M, Fay AM, Sullivan DA.
Schepens Eye Research Institute.