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doi:10.1016/j.exger.2010.03.002


Thema: 11/ibapublikationen
Institut für Biomedizinische Alternsforschung


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T. Diener, M. Neuhaus, R. Koziel, L. Micutkova, P. Jansen-Dürr
S.  638 - 644
Open access
doi:10.1016/j.exger.2010.03.002
Abstract:
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.

Keywords:  HUVEC EndoG Senescence Apoptosis
Published Online:  2011/11/23 14:29:37
Object Identifier:  0xc1aa5576 0x0029dc75



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epub.oeaw – Institutionelles Repositorium der Österreichischen Akademie der Wissenschaften
epub.oeaw – Institutional Repository of the Austrian Academy of Sciences
A-1011 Wien, Dr. Ignaz Seipel-Platz 2
Tel. +43-1-515 81/DW 3402-3406, Fax +43-1-515 81/DW 3400
http://epub.oeaw.ac.at, e-mail: epub@oeaw.ac.at