| Aging of different avian cultured cells: lack of ROS-induced damage and quality control mechanisms. | |
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MedLine Citation:
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PMID: 19948180 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Elevated reactive oxygen species (ROS) levels have been observed in mammals during aging, implying an important role of ROS in the aging process. Most bird species are known to live longer and to contain lower ROS levels than mammals of the same body weight. The influence of ROS on the aging process of birds has been investigated using pigeon embryonic fibroblasts (PEF) and chicken embryonic fibroblasts (CEF). ROS levels in young avian cells were much lower than in human cells. When cultivated till replicative senescence, PEF proliferated about one-third longer compared to CEF. However, both senescent avian cell populations showed no increased ROS levels or accumulation of ROS-induced damage on the mtDNA or protein level. The investigation for quality control (QC) mechanisms revealed that the autophagosomal/lysosomal pathway was not downregulated in old avian cells and stable overexpression of the autophagy protein ATG5 improved mitochondrial fitness, enhanced the resistance against oxidative stress and prolonged the life span of CEF. Oxidative stress-mediated apoptosis induced a dose-dependent cell proliferation in CEF as well as in PEF. Taken together, our data indicate that autophagy and compensatory proliferation act as QC mechanisms, while ROS did not influence the aging process in avian cells. |
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Authors:
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Valentina Strecker; S?ren Mai; Britta Muster; Sascha Beneke; Alexander B?rkle; J?rgen Bereiter-Hahn; Marina Jendrach |
Publication Detail:
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Type: Comparative Study; Journal Article; Research Support, Non-U.S. Gov't Date: 2009-12-03 |
Journal Detail:
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Title: Mechanisms of ageing and development Volume: 131 ISSN: 1872-6216 ISO Abbreviation: Mech. Ageing Dev. Publication Date: 2010 Jan |
Date Detail:
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Created Date: 2010-01-29 Completed Date: 2010-04-02 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 0347227 Medline TA: Mech Ageing Dev Country: Ireland |
Other Details:
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Languages: eng Pagination: 48-59 Citation Subset: IM |
Affiliation:
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Kinematic Cell Research Group, Institute for Cell Biology and Neuroscience, Center of Excellence Frankfurt: Macromolecular Complexes, Goethe University, Max-von-Laue-Str. 9, 60438 Frankfurt/Main, Germany. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Autophagy* / genetics Cell Aging* / genetics Cell Proliferation* Cell Survival Cells, Cultured Chick Embryo Columbidae DNA Damage DNA, Mitochondrial / metabolism Fibroblasts / metabolism*, pathology Lysosomes / metabolism Microtubule-Associated Proteins / genetics, metabolism Oxidative Stress* Protein Carbonylation Reactive Oxygen Species / metabolism* Transfection |
| Chemical | |
Reg. No./Substance:
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0/DNA, Mitochondrial; 0/Microtubule-Associated Proteins; 0/Reactive Oxygen Species |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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