Purchase this article with an account.
F. Schirra, J. Scheidt, Z. Gatzioufas, B. Seitz; Testosterone Down-Regulates Keratinization in the Mouse Meibomian Gland. Invest. Ophthalmol. Vis. Sci. 2008;49(13):93. doi: https://doi.org/.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
Exaggerated keratinization appears to play a major role in the dysfunction of the meibomian gland. This work displays the impact of androgens on limiting keratinization in this tissue, thus, contributing to normal meibomian gland function and ocular surface health.
Orchiectomized mice were systemically treated with either testosterone or placebo for two weeks. The mRNA was then extracted from the meibomian glands and differential gene expression was investigated by microarray hybridisation and evaluation with GeneSifter software as well as gene ontology information of the Gene Ontology (GO) Consortium.
By z-score calculation, keratinization was the most significantly testosterone-influenced gene ontology term 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. Apart from keratinization, these genes are variably involved in epidermis development, keratinocyte differentiation, regulation of cell shape, cell morphogenesis, epithelial morphogenesis, and intermediate filament organization.
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 margin. Our findings elucidate, at least in part, the beneficial impact of androgens on meibomian gland function, and thus, on ocular surface health.
This PDF is available to Subscribers Only