Abstract
Purpose :
Age-related vitreoretinal interface diseases idiopathic epiretinal membrane (iERM) and macular hole (iMH) are potentially sight-threatening posterior segment eye diseases. Deeper understanding of biomechanical mechanisms and signaling pathways involved in these eye diseases is warranted. So far, vitreous proteomes of iERM and iMH remain largely unstudied.
Methods :
An institutional study. We performed liquid chromatography mass spectrometry (LC-MS) based label-free quantitative proteomics analysis of vitreous humor samples from patients with iERM (n=26), iMH (n=21), and type 2 diabetic macular edema (DME, n=7).
Results :
We identified 1014 and quantified the abundancy of 934 vitreous proteins. Gene Ontology (GO) analysis suggested that most of the iERM and iMH proteins were extracellular and transmembrane. 160 proteins differed between iERM and iMH groups (Q-value < 0.05), with 53 proteins being upregulated in iERM and 65 in iMH. Upregulated proteins in the iERM and MH iproteomes associate with similar biological processes, including cell adhesion, nervous system development and cell signaling. Also, specific processes were detected such as Wnt signaling for iERM as well as proteolysis and semaphorin-plexin pathway for MH. Interesting novel markers in iERM were caspase-5, fibulin-7, and tyrosinase. However, validation of these biomarkers remains a significant challenge.
Conclusions :
Bioinformatic analysis revealed that neurodegeneration rather than neuroinflammation seems to play an important role in the pathogenesis of iERM and iMH. The identification of the key signaling pathways and novel vitreous biomarkers of both iERM and iMH is critical for providing novel candidate targets for diagnostic and therapeutic approaches.
This is an abstract that was submitted for the 2018 ARVO Annual Meeting, held in Honolulu, Hawaii, April 29 - May 3, 2018.