Mitochondrial damage and cholesterol storage in human hepatocellular carcinoma cells with silencing of UBIAD1 gene expression

被引：7

作者：

Morales, Carlos R. ^{[1
]}

Grigoryeva, Lubov S. ^{[2
]}

Pan, Xuefang ^{[2
]}

Bruno, Luigi ^{[2
]}

Hicksonb, Gilles ^{[2
,4
,7
]}

Ngo, Michael H. ^{[3
]}

McMaster, Christopher R. ^{[3
]}

Samuels, Mark E. ^{[2
,4
]}

Pshezhetsky, Alexey V. ^{[1
,2
,5
,6
]}

机构：

[1] McGill Univ, Fac Med, Dept Anat & Cell Biol, Montreal, PQ, Canada

[2] CHU Sainte Justine Res Ctr, Montreal, PQ, Canada

[3] Dalhousie Univ, Dept Pharmacol, Halifax, NS, Canada

[4] Univ Montreal, Dept Med, Montreal, PQ, Canada

[5] Univ Montreal, Dept Pediat, Montreal, PQ, Canada

[6] Univ Montreal, Dept Biochem, Montreal, PQ, Canada

[7] Univ Montreal, Dept Pathol & Cell Biol, Montreal, PQ, Canada

来源：

MOLECULAR GENETICS AND METABOLISM REPORTS | 2014年 / 1卷

基金：

加拿大健康研究院;

关键词：

Mitochondrion; Reactive oxygen species; Cholesterol; CoQ10; Schnyder corneal dystrophy;

D O I：

10.1016/j.ymgmr.2014.09.001

中图分类号：

Q3 [遗传学];

学科分类号：

071007 ; 090102 ;

摘要：

Heterozygous mutations in the UBIAD1 gene cause Schnyder corneal dystrophy characterized by abnormal cholesterol and phospholipid deposits in the cornea. Ubiad1 protein was recently identified as Golgi prenyltransferase responsible for biosynthesis of vitamin K2 and CoQ10, a key protein in the mitochondrial electron transport chain. Our study shows that silencing UBIAD1 in cultured human hepatocellular carcinoma cells causes dramaticmorpho-logical changes and cholesterol storage in the mitochondria, emphasizing an important role of UBIAD1 in mitochondrial function. (C) 2014 The Authors. Published by Elsevier Inc. This is an open access article under the CC BY-NC-ND license

引用

页码：407 / 411

页数：5

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