Copenhagen 2016 Registration Programme Exhibitor Information Virtual Exhibition Satellite Meetings Glaucoma Day 2016 Hotel Star Alliance
title

10 - 14 Sept. 2016, Bella Center, Copenhagen, Denmark

This Meeting has been awarded 27 CME credits

 

escrs app advert yo advert

Comparative proteome analysis of the tear samples obtained from mild grade keratoconus (KC) patients

Search Title by author or title

Session Details

Session Title: Cornea Medical I

Session Date/Time: Monday 12/09/2016 | 17:00-18:30

Paper Time: 18:12

Venue: Hall C2

First Author: : F.Yenihayat TURKEY

Co Author(s): :    F. Yenihayat   O. Altintas   M. Kasap   N. Guzel   G. Akpinar   O. Celik     

Abstract Details

Purpose:

To obtain clues about the metabolic processes playing roles in formation of keratoconus (KC) using comperative DIGE-based proteomics approaches.

Setting:

prospective, case-controlled study

Methods:

Tears were collected using capillary glass tubes without prior anesthesia and stimulation from 17 patients and 16 controls. Proteomics analysis by fluorescent 2D gel electrophoresis (DIGE) coupled with MALDI-TOF/TOF was performed. The identified protein spots were subjected to Ingenuity Patway Analysis (IPA). Corneal topography analysis with Sirius topography system (Costruzioni Strumenti Oftalmici, Florence, Italy) were performed on all participants. The steepest keratometry index was lower than 50 diopters in all keratoconus patients.

Results:

DIGE analysis showed changes in abundance of nine proteins which were identified by MALDI-TOF/TOF analyses in the tear samples obtained from KC patients. Six of these proteins (Serum albumin, Keratin Type II Cytoskeletal 1, IgG gamma chain, GAPDH, Alpha-1 anti-trypsin and ApoA-I) were down regulated in KC samples in comparison to the controls. In addition, we detected upregulation of Lysozyme, Keratin Type I cytoskletal 10 and Lipocalin. The subsequent IPA analysis predicted that NADH repair pathway is activated in KC patients. This pathway involves generation of NADHX as a by-product via catalysis by GAPDH. NADHX is an inhibitor of several dehydrogenases and must be removed.

Conclusions:

The involvement of NADH repair pathway in KC should be investigated, since preliminary clues obtained in this study point to that direction.

Financial Disclosure:

NONE

Back to previous