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Fibroblasts from long‐lived mutant mice exhibit increased autophagy and lower TOR activity after nutrient deprivation or oxidative stress
Abstract
Summary: Previous work has shown that primary skin‐derived fibroblasts from long‐lived pituitary dwarf mutants resist the lethal effects of many forms of oxidative and nonoxidative stress. We hypothesized that increased autophagy may protect fibroblasts of Pit‐1 dw/dw (Snell dwarf) mice from multiple forms of stress. We found that dwarf‐derived fibroblasts had higher levels of autophagy, using LC3 and p62 as markers, in response to amino acid deprivation, hydrogen peroxide, and paraquat. Fibroblasts from dwarf mice also showed diminished phosphorylation of mTOR, S6K, and 4EBP1, consistent with the higher levels of autophagy in these cells after stress. Similar results were also observed in fibroblasts from mutant mice lacking growth hormone receptor (GHRKO mice) after amino acid withdrawal. Our results suggested that increased autophagy, regulated by TOR‐dependent processes, may contribute to stress resistance in fibroblasts from long‐lived mutant mice.
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“In mammals, autophagy is reportedly upregulated in CR mice and in the cells of long-lived Snell dwarf mice, and is required for some of the beneficial effects of a CR diet on the heart, kidney, and liver 69–72.”
From Targeting the biology of aging with mTOR inhibitors (2023) · cites this paper as [72]
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Metadata
- Authors
- Wang, M., & Miller, R. A.
- Venue
- Aging Cell
- Publisher
- Wiley
- Published
- 2012-06-04
- Volume
- 11
- Issue
- 4
- Pages
- 668-674
- ISSN
- 1474-9718
- 1474-9726
- PMC
- PMC3399977
- Cited by
- 45
- References
- 8
- Language
- en
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