| Role of endonuclease G in senescence-associated cell death of human endothelial cells. | |
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MedLine Citation:
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PMID: 20211237 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Mitotic cells in culture show a limited replicative potential and after extended subculturing undergo a terminal growth arrest termed cellular senescence. When cells reach the senescent phenotype, this is accompanied by a significant change in the cellular phenotype and massive changes in gene expression, including the upregulation of secreted factors. In human fibroblasts, senescent cells also acquire resistance to apoptosis. In contrary, in human endothelial cells, both replicative and stress-induced premature senescence is accompanied by increased cell death; however mechanisms of cell death are poorly explored. In this communication, we addressed the role of endonuclease G (EndoG), a mitochondrial mediator of caspase-independent cell death, in senescence-associated cell death of human endothelial cells. Using immunofluorescence microscopy, we found, that EndoG is localized in the mitochondria in young cells, but relocalizes to the nucleus upon senescence. When EndoG gene expression was downregulated by lentiviral shRNA vectors, we found a significant reduction in the replicative life span and a corresponding increase in cell death. We also observed a slight shift in the cell death phenotype from necrosis to apoptosis. Together these observations suggest an important role of EndoG in the senescence program of human endothelial cells. |
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Authors:
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Thomas Diener; Michael Neuhaus; Rafal Koziel; Lucia Micutkova; Pidder Jansen-Dürr |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2010-03-06 |
Journal Detail:
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Title: Experimental gerontology Volume: 45 ISSN: 1873-6815 ISO Abbreviation: Exp. Gerontol. Publication Date: 2010 Aug |
Date Detail:
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Created Date: 2010-06-01 Completed Date: 2010-09-14 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 0047061 Medline TA: Exp Gerontol Country: England |
Other Details:
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Languages: eng Pagination: 638-44 Citation Subset: IM |
Copyright Information:
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Copyright (c) 2010 Elsevier Inc. All rights reserved. |
Affiliation:
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Institute for Biomedical Aging Research, Austrian Academy of Sciences, Rennweg 10, Innsbruck, Austria. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Active Transport, Cell Nucleus Aging / genetics, metabolism Apoptosis / genetics*, physiology* Cell Aging / genetics*, physiology* Cells, Cultured Endodeoxyribonucleases / antagonists & inhibitors, genetics*, metabolism* Endothelial Cells / cytology*, enzymology* Gene Expression Gene Knockdown Techniques Humans Lentivirus / genetics Membrane Potential, Mitochondrial Necrosis / enzymology, genetics, pathology RNA, Small Interfering / genetics |
| Chemical | |
Reg. No./Substance:
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0/RNA, Small Interfering; EC 3.1.-/Endodeoxyribonucleases; EC 3.1.21.-/endonuclease G |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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