Disruptions of Autophagy in the Rat Retina with Age During the Development of Age-Related-Macular-Degeneration-like Retinopathy.
Oyuna S KozhevnikovaDarya V TeleginaMikhail A TyumentsevNataliya G KolosovaPublished in: International journal of molecular sciences (2019)
Age-related macular degeneration (AMD) is one of the main causes of vision impairment in the elderly. Autophagy is the process of delivery of cytoplasmic components into lysosomes for cleavage; its age-related malfunction may contribute to AMD. Here we showed that the development of AMD-like retinopathy in OXYS rats is accompanied by retinal transcriptome changes affecting genes involved in autophagy. These genes are associated with kinase activity, immune processes, and FoxO, mTOR, PI3K-AKT, MAPK, AMPK, and neurotrophin pathways at preclinical and manifestation stages, as well as vesicle transport and processes in lysosomes at the progression stage. We demonstrated a reduced response to autophagy modulation (inhibition or induction) in the OXYS retina at age 16 months: expression of genes Atg5, Atg7, Becn1, Nbr1, Map1lc3b, p62, and Gabarapl1 differed between OXYS and Wistar (control) rats. The impaired reactivity of autophagy was confirmed by a decreased number of autophagosomes under the conditions of blocked autophagosome-lysosomal fusion according to immunohistochemical analysis and transmission electron microscopy. Thus, the development of AMD signs occurs against the background of changes in the expression of autophagy-related genes and a decrease in autophagy reactivity: the ability to enhance autophagic flux in response to stress.
Keyphrases
- signaling pathway
- age related macular degeneration
- cell death
- pi k akt
- endoplasmic reticulum stress
- oxidative stress
- cell cycle arrest
- poor prognosis
- genome wide
- cell proliferation
- diabetic retinopathy
- high resolution
- electron microscopy
- dna methylation
- mesenchymal stem cells
- tyrosine kinase
- protein kinase
- rna seq
- optic nerve
- binding protein
- stress induced
- genome wide analysis