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Role of p53 in the cellular response following oleic acid accumulation in Chang liver cells.

Toxicology letters (2013-10-15)
Eun-Jung Park, Ah Young Lee, Seung-Hee Chang, Kyeong-Nam Yu, Jae-Ho Kim, Myung-Haing Cho
ABSTRACT

Abnormal accumulation of fatty acids triggers the harmful cellular response called lipotoxicity. In this study, we investigated the cellular response following accumulation of oleic acid (OA), a monounsaturated fatty acid, in human Chang liver cells. OA droplets were distributed freely in the cytoplasm and/or degraded within lysosomes. OA exposure increased ATP production and concomitantly dilated mitochondria. At 24h after OA exposure, cell viability decreased slightly and was coupled with a reduction in mitochondrial Ca(2+) concentration, the alteration in cell viability was also associated with the generation of reactive oxygen species and changes in the cell cycle. Moreover, OA treatment increased the expression of autophagy- and apoptotic cell death-related proteins in a dose-dependent manner. Furthermore, we investigated the role of p53, a tumor suppressor protein, in the cellular response elicited by OA accumulation. OA-induced changes in cell viability and ATP production were rescued to control levels when cells were pretreated with pifithrin-alpha (PTA), a p53 inhibitor. By contrast, the expressions of LC3-II and perilipin, proteins required for lipophagy, were down-regulated by PTA pretreatment. Taken together, our results suggest that p53 plays a key role in the cellular response elicited by OA accumulation in Chang liver cells.

MATERIALS
Product Number
Brand
Product Description

Supelco
Oleic acid, analytical standard
Sigma-Aldrich
Oleic acid, meets analytical specification of Ph, Eur., 65.0-88.0% (GC)
Sigma-Aldrich
Oleic acid, suitable for cell culture, BioReagent
Sigma-Aldrich
Oleic acid, ≥99% (GC)
Sigma-Aldrich
Oleic acid, natural, FCC
Supelco
Oleic acid, Selectophore, ≥99.0%
Sigma-Aldrich
Oleic acid, technical grade, 90%