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...

Full description

Bibliographic Details
Main Authors: Pardis Kaynezhad, Ilias Tachtsidis, Asmaa Aboelnour, Sobha Sivaprasad, Glen Jeffery
Format: Article
Language:English
Published: Nature Publishing Group 2021-02-01
Series:Scientific Reports
Online Access:https://doi.org/10.1038/s41598-021-82811-2
id doaj-bafd7149bf074acab8a4eb268d5549a8
record_format Article
spelling 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
collection 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
work_keys_str_mv AT pardiskaynezhad watchingsynchronousmitochondrialrespirationintheretinaanditsinstabilityinamousemodelofmaculardegeneration
AT iliastachtsidis watchingsynchronousmitochondrialrespirationintheretinaanditsinstabilityinamousemodelofmaculardegeneration
AT asmaaaboelnour watchingsynchronousmitochondrialrespirationintheretinaanditsinstabilityinamousemodelofmaculardegeneration
AT sobhasivaprasad watchingsynchronousmitochondrialrespirationintheretinaanditsinstabilityinamousemodelofmaculardegeneration
AT glenjeffery watchingsynchronousmitochondrialrespirationintheretinaanditsinstabilityinamousemodelofmaculardegeneration
_version_ 1724270209172242432