Upregulation of TFAM and mitochondria copy number in human lymphoblastoid cells

被引：25

作者：

Chakrabarty, Sanjiban ^{[1
]}

D'Souza, Reena Reshma ^{[1
]}

Kabekkodu, Shama Prasada ^{[1
]}

Gopinath, Puthiya M. ^{[1
]}

Rossignol, Rodrigue ^{[2
]}

Satyamoorthy, Kapaettu ^{[1
]}

机构：

[1] Manipal Univ, Manipal Life Sci Ctr, Div Biotechnol, Manipal 576104, Karnataka, India

[2] Univ Victor Segalen Bordeaux 2, INSERM, U688 Physiopathol Mitochondriale, F-33076 Bordeaux, France

来源：

MITOCHONDRION | 2014年 / 15卷

关键词：

Mitochondria; Lymphoblastoid cell lines; Copy number; TEAM; EPSTEIN-BARR-VIRUS; TRANSCRIPTION FACTOR-A; CRYOPRESERVED ISOLATED LYMPHOCYTES; NUCLEAR ANTIGEN-1; OXIDATIVE DAMAGE; REPAIR ACTIVITY; DNA; LINES; EXPRESSION; GENOME;

D O I：

10.1016/j.mito.2014.01.002

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Mitochondria are central to several physiological and pathological conditions in humans. In the present study, we performed copy number analysis of nuclear encoded mitochondrial genes, in peripheral blood mononuclear cells (PBMCs) and its representative lymphoblastoid cells (LCLs). We have observed hyper diploid copies of mitochondrial transcription factor A (TFAM) gene in the LCLs along with increased mtDNA copy number, mitochondrial mass, intracellular ROS and mitochondrial membrane potential, suggesting elevated mitochondrial biogenesis in LCLs. Gene expression analysis confirmed TFAM over-expression in LCLs when compared to PBMC. Based on our observation, we suggest that increased copy number of TFAM gene upregulates its expression, increases mtDNA copy numbers and protects it from oxidative stress induced damage in the transformed LCLs. (C) 2014 Elsevier B.V. and Mitochondria Research Society. All rights reserved.

引用

页码：52 / 58

页数：7

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