Abstract
Purpose :
The long-term prognosis of corneal transplantation is poor in eyes with complicated pseudophakic bullous keratopathy (PBK), especially eyes with a history of multiple intraocular surgeries. We recently demonstrated that higher levels of specific cytokines in the aqueous humor (AqH) are associated with the rapid reduction of corneal endothelial cell loss after corneal transplantation. However, its exact mechanism is still poorly understood. We comprehensively evaluated AqH protein levels using proteomic analysis in patients with PBK and Fuchs endothelial corneal dystrophy (FECD).
Methods :
We collected 100-200 μl AqH from cataract patients without any ocular comorbidities (5 eyes) and bullous keratopathy (5 eyes with PBK and 5 eyes with FECD) at the beginning of cataract surgery or endothelial keratoplasty. Proteomic analysis was conducted using Orbitrap Fusion Lumos. Gene ontology (GO) analysis was applied to the proteins which elevated only in PBK eyes, compared to cataract eyes and FECD eyes with P values less than P<0.001.
Results :
The levels of 1162 proteins in the AqH were successfully quantified. Compared to cataract eyes, 69 proteins elevated only in PBK eyes, 35 proteins elevated only in FECD eyes and 33 proteins both in PBK and FECD eyes (P<0.001). Out of 30 elevated proteins only in PBK eyes (P<0.0001), 16 proteins were those related to complement pathways. Some molecules which modulate or inhibit complement systems were significantly downregulated in eyes with PBK. GO analysis showed that complement activation is the major pathway in PBK.
Conclusions :
Among extensive alterations in AqH protein levels in eyes with bullous keratopathy, complement activation was identified as one of the major pathways in PBK eyes.
This is an abstract that was submitted for the 2018 ARVO Annual Meeting, held in Honolulu, Hawaii, April 29 - May 3, 2018.