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AUTOPHAGY IN DNA DAMAGE INDUCED ACCELERATED AGING

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Date Issued:
2017
Abstract/Description:
Autophagy, the cellular “recycling system” of unnecessary components, is a crucial mechanism for maintaining homeostasis inside the cell. Whereas impaired DNA repair function leads to accelerated aging and an early onset of several age-related diseases, it is not known whether autophagy plays a mediating role in this process. Here, we examined changes in autophagy in cells with progeria due to a disabled ERCC1-XPF, a nuclear DNA repair enzyme. We found that loss of ERCC1 function leads to DNA damage and a decrease in autophagic flux in cells. Low dose treatment with Rapamycin, an autophagy inducer, improved proliferation and delayed aging, or cellular senescence, in the cells. These data suggest that persistent DNA damage suppresses autophagic flux, thus contributing to early senescence and accelerated onset of age-related diseases. Therefore, therapeutics that improve autophagic flux, may prove beneficial for progeroid patients.
Title: AUTOPHAGY IN DNA DAMAGE INDUCED ACCELERATED AGING.
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Name(s): Muravia, Mariya , author
Wetterer, James K., Thesis advisor
Florida Atlantic University, Degree Grantor
Harriet L. Wilkes Honors College
Type of Resource: text
Genre: Thesis
Date Created: 2017
Date Issued: 2017
Publisher: Florida Atlantic University
Place of Publication: Jupiter, Florida
Physical Form: application/pdf
Extent: 29 p.
Language(s): English
Abstract/Description: Autophagy, the cellular “recycling system” of unnecessary components, is a crucial mechanism for maintaining homeostasis inside the cell. Whereas impaired DNA repair function leads to accelerated aging and an early onset of several age-related diseases, it is not known whether autophagy plays a mediating role in this process. Here, we examined changes in autophagy in cells with progeria due to a disabled ERCC1-XPF, a nuclear DNA repair enzyme. We found that loss of ERCC1 function leads to DNA damage and a decrease in autophagic flux in cells. Low dose treatment with Rapamycin, an autophagy inducer, improved proliferation and delayed aging, or cellular senescence, in the cells. These data suggest that persistent DNA damage suppresses autophagic flux, thus contributing to early senescence and accelerated onset of age-related diseases. Therefore, therapeutics that improve autophagic flux, may prove beneficial for progeroid patients.
Identifier: FA00012630 (IID)
Degree granted: Thesis (B.A.)--Florida Atlantic University, Harriet L. Wilkes Honors College, 2017.
Collection: FAU Honors Theses Digital Collection
Note(s): Includes bibliography.
Held by: Florida Atlantic University Libraries
Sublocation: Digital Library
Persistent Link to This Record: http://purl.flvc.org/fau/fd/FA00012630
Use and Reproduction: Copyright © is held by the author with permission granted to Florida Atlantic University to digitize, archive and distribute this item for non-profit research and educational purposes. Any reuse of this item in excess of fair use or other copyright exemptions requires permission of the copyright holder.
Host Institution: FAU
Is Part of Series: Florida Atlantic University Digital Library Collections.

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