DJ-1 deficiency alleviates steatosis in cultured hepatocytes

被引:0
作者
Chaudhari, Harmesh N. [1 ]
Yun, Jong Won [1 ]
机构
[1] Daegu Univ, Dept Biotechnol, Kyungsan 712714, South Korea
关键词
C9; DJ-1; lipolysis; mitochondria; steatosis; GENDER-DIMORPHIC REGULATION; BINDING-PROTEIN-BETA; FATTY LIVER-DISEASE; HEPATIC STEATOSIS; INSULIN-RESISTANCE; MOUSE MODEL; PPAR-GAMMA; MICE; DIET; METABOLISM;
D O I
10.1007/s12257-015-0689-5
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
Imbalance in lipid metabolism within hepatocytes can lead to hepatosteatosis, which is a cause of numerous hepatic dysfunctions. Previous studies have demonstrated the roles of DJ-1 in Parkinson's disease, diet-induced oxidative stress, obesity, and diabetes. Although recent studies have shown that DJ-1 is involved in metabolic complications, the roles of DJ-1 in steatosis are largely unknown. Therefore, the aim of the current study was to elucidate the potential roles of DJ-1 in hepatosteatosis in vitro. Normal rat liver cells Clone 9 (C9) were treated with 1 mM oleic acid (OA) for 24 h for establishment of a steatosis model, after which various biochemical parameters, including triglyceride, total cholesterol, and free fatty acid contents, were determined after knockdown with Dj1- specific siRNA. Silencing of Dj1 prevented hepatic steatosis by suppressing expression of hepatic lipogenic markers, which was confirmed by immunoblotting and real-time PCR analysis. Up-regulation of mitochondrial and beta- oxidation-associated proteins showed potential to reduce fat accumulation in the liver. Silencing of Dj1 resulted in alleviation of steatosis by reducing lipogenesis and improving mitochondrial biogenesis. Further in vivo studies will be required to understand the molecular mechanism behind the role of DJ-1 in steatosis.
引用
收藏
页码:1152 / 1161
页数:10
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