Please use this identifier to cite or link to this item: https://doi.org/10.18632/aging.103740
Title: Decreased autophagy and fuel switching occur in a senescent hepatic cell model system
Authors: Singh, Brijesh Kumar 
Tripathi, Madhulika 
Sandireddy, Reddemma 
Tikno, Keziah 
Zhou, Jin 
Yen, Paul Michael 
Keywords: Science & Technology
Life Sciences & Biomedicine
Cell Biology
Geriatrics & Gerontology
aging
liver
senescence
metabolism
AML12 cells
Issue Date: 31-Jul-2020
Publisher: IMPACT JOURNALS LLC
Citation: Singh, Brijesh Kumar, Tripathi, Madhulika, Sandireddy, Reddemma, Tikno, Keziah, Zhou, Jin, Yen, Paul Michael (2020-07-31). Decreased autophagy and fuel switching occur in a senescent hepatic cell model system. AGING-US 12 (14) : 13958-13978. ScholarBank@NUS Repository. https://doi.org/10.18632/aging.103740
Abstract: Although aging in the liver contributes to the development of chronic liver diseases such as NAFLD and insulin resistance, little is known about the molecular and metabolic details of aging in hepatic cells. To examine these issues, we used sequential oxidative stress with hydrogen peroxide to induce premature senescence in AML12 hepatic cells. The senescent cells exhibited molecular and metabolic signatures, increased SA-βGal and γH2A. X staining, and elevated senescence and pro-inflammatory gene expression that resembled livers from aged mice. Metabolic phenotyping showed fuel switching towards glycolysis and mitochondrial glutamine oxidation as well as impaired energy production. The senescent AML12 cells also had increased mTOR signaling and decreased autophagy which likely contributed to the fuel switching from β-oxidation that occurred in normal AML12 cells. Additionally, senescence-associated secretory phenotype (SASP) proteins from conditioned media of senescent cells sensitized normal AML12 cells to palmitate-induced toxicity, a known pathological effect of hepatic aging. In summary, we have generated senescent AML12 cells which displayed the molecular hallmarks of aging and also exhibited the aberrant metabolic phenotype, mitochondrial function, and cell signaling that occur in the aged liver.
Source Title: AGING-US
URI: https://scholarbank.nus.edu.sg/handle/10635/226723
ISSN: 19454589
DOI: 10.18632/aging.103740
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