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Mario Matthaei, Christoph Leitl, Rebecca Scholz, Björn Bachmann, Thomas Langmann, Claus Cursiefen, Ludwig M Heindl; Correlation of extracellular matrix-related gene expression with objective Fuchs Endothelial Corneal Dystrophy severity. Invest. Ophthalmol. Vis. Sci. 2016;57(12):5275.
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© ARVO (1962-2015); The Authors (2016-present)
Fuchs Endothelial Corneal Dystrophy (FECD) is characterized by accelerated decrease in corneal endothelial cell (CEC) density and excessive subendothelial deposition of extracellular matrix (ECM). The present study aimed to analyze if the expression-levels of individual ECM-related genes in CECs correlate with objective disease severity of FECD patients.
Included FECD patients (n=42, mean age ± SD: 69±9) underwent Descemet membrane endothelial keratoplasty (DMEK) surgery at the Department of Ophthalmology, University of Cologne, Cologne, Germany. Patients underwent routine clinical slit-lamp examination before surgery. Corneal central-to-peripheral thickness ratio at 3.5 mm from the center (CPTR3.5) was determined by slit scanning pachymetry as an objective metric for FECD severity. Corneal endothelial samples from FECD eyes were obtained during DMEK surgery. Expression of ECM-related genes (COL1A1, COL3A1, COL4A1, FN1, LAMC1) was measured using Taqman qPCR. Correlation coefficient r and P values were calculated by Spearman correlation.
Mean peripheral corneal thickness at 3.5mm from the center (PCT3.5) ± SD was 700 ± 43µm (mean corneal thickness ± SD: superior 700 ± 42µm, inferior 712 ± 49µm, nasal 684 ± 56µm, temporal 702 ± 61µm). Mean central corneal thickness (CCT) ± SD was 720 ± 61µm. Mean CPTR3.5 ± SD was 1.03 ± 0.06. A correlation between CPTR3.5 and mRNA expression-levels was found for COL1A1, COL4A1, LAMC1 and FN1 with FN1 showing the most prominent correlation with CPTR3.5 (Spearman r = 0.45; p<0.01).
The present study provides evidence that objective FECD severity as measured by CPTR3.5 is positively correlated with expression of individual ECM-related genes in corneal endothelial cells. Further studies need to clarify if these ECM-related genes may serve as targets/markers for future conservative FECD treatment strategies.
This is an abstract that was submitted for the 2016 ARVO Annual Meeting, held in Seattle, Wash., May 1-5, 2016.
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