Mitochondrial contribution to lipofuscin formation
Mitochondria have been in the focus of oxidative stress and aging research for decades due to their permanent production of ROS during the oxidative phosphorylation. The hypothesis exists that mitochondria are involved in the formation of lipofuscin, an autofluorescent protein aggregate that accumul...
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doaj-fed2184c83f44ab782e17121d15327292020-11-25T00:46:46ZengElsevierRedox Biology2213-23172017-04-0111673681Mitochondrial contribution to lipofuscin formationJeannette König0Christiane Ott1Martín Hugo2Tobias Jung3Anne-Laure Bulteau4Tilman Grune5Annika Höhn6Department of Molecular Toxicology, German Institute of Human Nutrition Potsdam-Rehbruecke (DIfE), 14558 Nuthetal, GermanyDepartment of Molecular Toxicology, German Institute of Human Nutrition Potsdam-Rehbruecke (DIfE), 14558 Nuthetal, GermanyDepartment of Molecular Toxicology, German Institute of Human Nutrition Potsdam-Rehbruecke (DIfE), 14558 Nuthetal, GermanyDepartment of Molecular Toxicology, German Institute of Human Nutrition Potsdam-Rehbruecke (DIfE), 14558 Nuthetal, Germany; German Center for Cardiovascular Research (DZHK), 10117 Berlin, GermanyInstitut de Génomique Fonctionnelle de Lyon (IGFL) – ENS de Lyon, 69007 Lyon, FranceDepartment of Molecular Toxicology, German Institute of Human Nutrition Potsdam-Rehbruecke (DIfE), 14558 Nuthetal, Germany; German Center for Diabetes Research (DZD), 85764 München-Neuherberg, Germany; German Center for Cardiovascular Research (DZHK), 10117 Berlin, Germany; NutriAct-Competence Cluster Nutrition Research Berlin-Potsdam, Nuthetal 14458, GermanyDepartment of Molecular Toxicology, German Institute of Human Nutrition Potsdam-Rehbruecke (DIfE), 14558 Nuthetal, Germany; German Center for Diabetes Research (DZD), 85764 München-Neuherberg, Germany; Correspondence to: German Institute of Human Nutrition Potsdam-Rehbruecke, Arthur-Scheunert-Allee 114-116, 14558 Nuthetal, GermanyMitochondria have been in the focus of oxidative stress and aging research for decades due to their permanent production of ROS during the oxidative phosphorylation. The hypothesis exists that mitochondria are involved in the formation of lipofuscin, an autofluorescent protein aggregate that accumulates progressively over time in lysosomes of post-mitotic and senescent cells. To investigate the influence and involvement of mitochondria in lipofuscinogenesis, we analyzed lipofuscin amounts as well as the mitochondrial function in young and senescent cells. In addition we used an aging model and Lon protease deficient HeLa cells to investigate the influence of mitochondrial degradation processes on lipofuscin formation.We were able to show that mitophagy is impaired in senescent cells resulting in an increased mitochondrial mass and superoxide formation. In addition, the inhibition of mitochondrial fission leads to increased lipofuscin formation.Moreover, we observed that Lon protease downregulation is linked to a higher lipofuscinogenesis whereas the application of the mitochondrial-targeted antioxidant mitoTEMPO is able to prevent the accumulation of this protein aggregate. Keywords: Lipofuscin, Protein aggregates, Lon protease, Aging, Mitochondria, Oxidative stresshttp://www.sciencedirect.com/science/article/pii/S2213231717300423 |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Jeannette König Christiane Ott Martín Hugo Tobias Jung Anne-Laure Bulteau Tilman Grune Annika Höhn |
spellingShingle |
Jeannette König Christiane Ott Martín Hugo Tobias Jung Anne-Laure Bulteau Tilman Grune Annika Höhn Mitochondrial contribution to lipofuscin formation Redox Biology |
author_facet |
Jeannette König Christiane Ott Martín Hugo Tobias Jung Anne-Laure Bulteau Tilman Grune Annika Höhn |
author_sort |
Jeannette König |
title |
Mitochondrial contribution to lipofuscin formation |
title_short |
Mitochondrial contribution to lipofuscin formation |
title_full |
Mitochondrial contribution to lipofuscin formation |
title_fullStr |
Mitochondrial contribution to lipofuscin formation |
title_full_unstemmed |
Mitochondrial contribution to lipofuscin formation |
title_sort |
mitochondrial contribution to lipofuscin formation |
publisher |
Elsevier |
series |
Redox Biology |
issn |
2213-2317 |
publishDate |
2017-04-01 |
description |
Mitochondria have been in the focus of oxidative stress and aging research for decades due to their permanent production of ROS during the oxidative phosphorylation. The hypothesis exists that mitochondria are involved in the formation of lipofuscin, an autofluorescent protein aggregate that accumulates progressively over time in lysosomes of post-mitotic and senescent cells. To investigate the influence and involvement of mitochondria in lipofuscinogenesis, we analyzed lipofuscin amounts as well as the mitochondrial function in young and senescent cells. In addition we used an aging model and Lon protease deficient HeLa cells to investigate the influence of mitochondrial degradation processes on lipofuscin formation.We were able to show that mitophagy is impaired in senescent cells resulting in an increased mitochondrial mass and superoxide formation. In addition, the inhibition of mitochondrial fission leads to increased lipofuscin formation.Moreover, we observed that Lon protease downregulation is linked to a higher lipofuscinogenesis whereas the application of the mitochondrial-targeted antioxidant mitoTEMPO is able to prevent the accumulation of this protein aggregate. Keywords: Lipofuscin, Protein aggregates, Lon protease, Aging, Mitochondria, Oxidative stress |
url |
http://www.sciencedirect.com/science/article/pii/S2213231717300423 |
work_keys_str_mv |
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