Abstract
Purpose :
Exfoliation syndrome (XFS) is an age-related systemic disorder involving the accumulation of amorphous protein aggregates within the extracellular matrix of many tissues, especially on the surface of the ciliary body, iris and lens. The autophagy dysfunction that causes a decrease in degradation of both denatured proteins and aging cellular organelles, may be thought to give rise to those aggregates in XFS. The aim of our study is to investigate different autophagy pathways and mitochondrial dysfunction in XFS.
Methods :
Anterior lens capsules derived from microincision cataract surgery with XFS (n=13) were collected and compared to anterior lens capsules of age-matched healthy controls (n=17). The samples were placed in RNAlater and stored at -80 °C until they were used. RNA isolation was done and measured with the NanoDrop. The reverse transcription- polymerase chain reaction (RT- PCR) was performed for PTEN- putative kinase 1 (PINK1), PARKIN, BNIP3, NIX and LC3A, LC3B, p62 gene expressions.
Results :
The mRNA expressions of PINK1, PARKIN and BNIP3 increased significantly in the lens epithelial cells with XFS compared to healthy controls (p<0.05), while the expression of NIX decreased significantly (p<0.05). The mRNA expressions of LC3A, LC3B and p62 were not significantly different in the samples with XFS compared to controls (p>0.05).
Conclusions :
In this study, we found that mitophagy pathways are impaired in the lens epithelial cells with XFS compared to controls. This deterioration may shed light on the pathogenesis of the disease in the light of the impairment of degradative process in specific autophagy pathways and mitochondrial dysfunction. Further studies are needed to evaluate the protein expressions of the above-mentioned genes.
This is a 2021 ARVO Annual Meeting abstract.