[Article in German]
Extensive keratinization appears to play a major role in the dysfunction of the Meibomian gland. This article presents the potential impact of androgens on limiting keratinization in this tissue, thus, contributing to normal Meibomian gland function and a healthy ocular surface.
MATERIALS AND METHODS:
Orchidectomized mice were systemically treated with either testosterone or placebo for 2 weeks. The mRNA was then extracted from the Meibomian glands and differential gene expression was investigated by microarray hybridization and evaluation with GeneSifter software as well as gene ontology information from the Gene Ontology (GO) Consortium.
By z-score calculations, keratinization was the most significantly gene ontology term influenced by testosterone based on down-regulated genes in the mouse Meibomian gland. In particular, under the influence of testosterone the genes coding for small proline-rich protein (Sprr) 2a, Sprr 2b, Sprr 3, keratins 6a and 17 and periplakin were significantly down-regulated, while Sprr 1a and Sprr 2f were significantly up-regulated.
Testosterone down-regulates the expression of genes promoting keratinization in the Meibomian gland. This may help to prevent Meibomian gland dysfunction by limiting excessive keratinization of this tissue and the adjacent lid margins. The findings elucidate, at least in part, the beneficial impact of androgens on Meibomian gland function and thus on the health of the ocular surface.
Ophthalmologe. 2012 Dec 8. [Epub ahead of print]
Schirra F, Gatzioufas Z, Scheidt J, Seitz B.
Klinik für Augenheilkunde, Universitätsklinikum des Saarlandes UKS, Kirrberger Str. 1, Geb. 22, 66421, Homburg/Saar, Deutschland, email@example.com.