Watching synchronous mitochondrial respiration in the retina and its instability in a mouse model of macular degeneration
Abstract 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...
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2021-02-01
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Online Access: | https://doi.org/10.1038/s41598-021-82811-2 |
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doaj-bafd7149bf074acab8a4eb268d5549a82021-02-14T12:36:23ZengNature Publishing GroupScientific Reports2045-23222021-02-0111111110.1038/s41598-021-82811-2Watching synchronous mitochondrial respiration in the retina and its instability in a mouse model of macular degenerationPardis Kaynezhad0Ilias Tachtsidis1Asmaa Aboelnour2Sobha Sivaprasad3Glen Jeffery4Institute of Ophthalmology, University College LondonDepartment of Medical Physics and Biomedical Engineering, University College LondonHistology and Cytology Department, Faculty of Veterinary Medicine, Damanhour UniversityInstitute of Ophthalmology, University College LondonInstitute of Ophthalmology, University College LondonAbstract 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.https://doi.org/10.1038/s41598-021-82811-2 |
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DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Pardis Kaynezhad Ilias Tachtsidis Asmaa Aboelnour Sobha Sivaprasad Glen Jeffery |
spellingShingle |
Pardis Kaynezhad Ilias Tachtsidis Asmaa Aboelnour Sobha Sivaprasad Glen Jeffery Watching synchronous mitochondrial respiration in the retina and its instability in a mouse model of macular degeneration Scientific Reports |
author_facet |
Pardis Kaynezhad Ilias Tachtsidis Asmaa Aboelnour Sobha Sivaprasad Glen Jeffery |
author_sort |
Pardis Kaynezhad |
title |
Watching synchronous mitochondrial respiration in the retina and its instability in a mouse model of macular degeneration |
title_short |
Watching synchronous mitochondrial respiration in the retina and its instability in a mouse model of macular degeneration |
title_full |
Watching synchronous mitochondrial respiration in the retina and its instability in a mouse model of macular degeneration |
title_fullStr |
Watching synchronous mitochondrial respiration in the retina and its instability in a mouse model of macular degeneration |
title_full_unstemmed |
Watching synchronous mitochondrial respiration in the retina and its instability in a mouse model of macular degeneration |
title_sort |
watching synchronous mitochondrial respiration in the retina and its instability in a mouse model of macular degeneration |
publisher |
Nature Publishing Group |
series |
Scientific Reports |
issn |
2045-2322 |
publishDate |
2021-02-01 |
description |
Abstract 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. |
url |
https://doi.org/10.1038/s41598-021-82811-2 |
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