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Tobias Weinrich Weinrich, Michael B. Powner, Glen Jeffery; Does S cone vulnerability reside in their mitochondria?. Invest. Ophthalmol. Vis. Sci. 2017;58(8):609.
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© ARVO (1962-2015); The Authors (2016-present)
We have recently provided evidence that there is little or no age related cone loss in the primate retina. However, there is differential loss of S cone function with age. Here we investigate molecular markers of cellular function and stress in aged S and M/L primate cones that may explain their differential decline.
Retinae from old Macaca fascicularis (14 y/o, n=6) were used, which had been donated at death in studies unrelated to our investigations. Data were also obtained from C57 mice retinae (n=10). We examined the localization and levels of DNA damage, protein aggregation and expression of mitochondrial stress markers in relation to the specific opsin expression. The localisation and expression studies were performed using immunohistochemistry (IHC) on retinal sections (macaque and mouse). Western blotting on frozen material was also used in the case of the mice, as the mouse retina has a clear dorso-ventral spatial separation of S and M/L cones.
We find differential changes in the level of protein aggregation in the outer segments of S-cone population compared to the M/L cone population, implying that cellular function has been undermined. In general, reactive oxygen species related DNA damage was present in all cones and other cell types. Co-labelling with specific S and M/L opsin revealed marginal differences between the S and M/L cone population in some of these metrics. However, there was an increased tendency of mitochondrial stress markers in the M/L cone population in comparison to the S-cone population implying that S cones may be less reliant on mitochondrial function.
These results suggest that there was not a significant differential difference in the metrics examined other than protein aggregation between the different cone types. However, it is possible S cone vulnerability may reside in their greater dependence on other energy source such as glycolysis rather than upon mitochondrial function. This may explain why S cone decline markedly in metabolic diseases.
This is an abstract that was submitted for the 2017 ARVO Annual Meeting, held in Baltimore, MD, May 7-11, 2017.
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