Impairment of Lon-Induced Protection Against the Accumulation of Oxidized Proteins in Senescent Wi-38 Fibroblasts
| Autor: | Daniela A. Bota, Kelvin J.A. Davies, Jenny K. Ngo, Alison L. Koop, Laura C.D. Pomatto |
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| Rok vydání: | 2011 |
| Předmět: |
Senescence
Aging Protease La Clinical Sciences Blotting Western Mitochondrion Biology medicine.disease_cause Mitochondrial Proteins Tumor Cells Cultured Journal of Gerontology: BIOLOGICAL SCIENCES medicine Humans Viability assay Fibroblast Cells Cultured Cellular Senescence Lon Proteolytic enzymes Fibroblasts Adaptation Physiological WI-38 Mitochondria Cell biology Oxidative Stress medicine.anatomical_structure Cell Aging Proteolysis bacteria Geriatrics and Gerontology Gerontology Cell aging Oxidative stress |
| Zdroj: | Ngo, Jenny K; Pomatto, Laura CD; Bota, Daniela A; Koop, Alison L; & Davies, Kelvin JA. (2011). Impairment of lon-induced protection against the accumulation of oxidized proteins in senescent wi-38 fibroblasts.. The journals of gerontology. Series A, Biological sciences and medical sciences, 66(11), 1178-1185. doi: 10.1093/gerona/glr145. UC Office of the President: Research Grants Program Office (RGPO). Retrieved from: http://www.escholarship.org/uc/item/6695c9sw |
| ISSN: | 1758-535X 1079-5006 |
| Popis: | Oxidative damage to mitochondrial proteins is thought to contribute to the aging process, but the Lon protease normally degrades such proteins. In early-passage WI-38 human lung fibroblasts, Lon expression is rapidly induced during H(2)O(2) stress, which prevents the accumulation of oxidized proteins and protects cell viability. In contrast, middle passage cells exhibit only sluggish induction of Lon expression in oxidative stress, and oxidized proteins initially accumulate. Late-passage, or senescent, cells have low basal levels of Lon and high levels of accumulated oxidized proteins; in response to oxidative stress, they fail to induce Lon expression and exhibit continually increasing accumulation of oxidized proteins. Senescent cells separated into two populations, one exhibiting normal mitochondrial mass and a second displaying significant loss of mitochondria; both populations had diminished mitochondrial transmembrane potential. These senescent changes are similar to the effects of Lon silencing in young cells. We suggest that loss of Lon stress inducibility is part of a pattern of diminishing stress adaptability that predisposes cells to senescence. |
| Databáze: | OpenAIRE |
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