Purchase this article with an account.
Edward J. Wladis, Supraja Swamy, Alyssa Herrmann, Jinhong Yang, J. Andrew Carlson, Alejandro P. Adam; Activation of p38 and Erk Mitogen-Activated Protein Kinases Signaling in Ocular Rosacea. Invest. Ophthalmol. Vis. Sci. 2017;58(2):843-848. doi: 10.1167/iovs.16-20275.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
Rosacea-related cutaneous inflammation is a common cause of ocular surface disease. Currently, there are no specific pharmacologic therapies to treat ocular rosacea. Here, we aimed at determining the differences in intracellular signaling activity in eyelid skin from patients with and without ocular rosacea.
This was an observational, comparative case series including 21 patients undergoing lower lid ectropion surgery at one practice during 2013 and 2014 (18 patients with rosacea, 13 control patients), and 24 paraffin-embedded archival samples from Albany Medical Center, selected randomly (12 patients with rosacea, 12 control patients). Cutaneous biopsies resulting from elective lower lid ectropion surgery were analyzed by Proteome Profiler Human Phospho-Kinase Array, Western blot, and/or immunohistochemistry.
Samples derived from ocular rosacea patients showed increased levels of phosphorylated (active) p38 and Erk kinases. Phosphoproteins were mainly localized to the epidermis of affected eyelids.
This finding provides a novel potential therapeutic target for treatment of ocular rosacea and possibly other forms of rosacea. Further testing is required to determine if p38 and Erk activation have a causal role in ocular rosacea. The selective activation of keratinocytes in the affected skin suggests that topical pathway inhibition may be an effective treatment that will ultimately prevent ocular surface damage due to ocular rosacea.
This PDF is available to Subscribers Only