Watching synchronous mitochondrial respiration in the retina and its instability in a mouse model of macular degeneration

• Published in: Scientific reports 2021-02, Vol.11 (1), p.3274-3274, Article 3274
• Main Authors: Kaynezhad, Pardis, Tachtsidis, Ilias, Aboelnour, Asmaa, Sivaprasad, Sobha, Jeffery, Glen
• Format: Article
• Language: English
• Subjects: 639/624/1107/527; 639/624/1111/55; Aging; Aging - genetics; Aging - metabolism; Animal models; Animals; Complement factor H; Disease Models, Animal; Hemodynamics; Humanities and Social Sciences; Macular degeneration; Macular Degeneration - genetics; Macular Degeneration - metabolism; Mice; Mice, Knockout; Mitochondria; Mitochondria - genetics; Mitochondria - metabolism; multidisciplinary; Oscillations; Oxygen Consumption; Oxygenation; Retina; Retina - metabolism; Science; Science (multidisciplinary)
• ISSN: 2045-2322; 2045-2322
• DOI: 10.1038/s41598-021-82811-2

Mitochondrial function declines with age and in some diseases, but we have been unable to analyze this in vivo. Here, we optically examine retinal mitochondrial function as well as choroidal oxygenation and hemodynamics in aging C57 and complement factor H (CFH −/− ) mice, proposed models of macular degeneration which suffer early retinal mitochondrial decline. In young C57s mitochondrial populations respire in coupled oscillatory behavior in cycles of ~ 8 min, which is phase linked to choroidal oscillatory hemodynamics. In aging C57s, the oscillations are less regular being ~ 14 min and more dissociated from choroidal hemodynamics. The mitochondrial oscillatory cycles are extended in CFH −/− mice being ~ 16 min and are further dissociated from choroidal hemodynamics. Mitochondrial decline occurs before age-related changes to choroidal vasculature, hence, is the likely origin of oscillatory disruption in hemodynamics. This technology offers a non-invasive technique to detect early retinal disease and its relationship to blood oxygenation in vivo and in real time.