Genomic and proteomic profiling of oxidative stress response in human diploid fibroblasts

被引:14
作者
Xie, Lifang [1 ]
Pandey, Ritu [2 ]
Xu, Beibei [1 ]
Tsaprailis, George [3 ]
Chen, Qin M. [1 ]
机构
[1] Univ Arizona, Dept Pharmacol, Coll Med, Tucson, AZ 85724 USA
[2] Arizona Canc Ctr, Tucson, AZ 85724 USA
[3] SW Environm Hlth Sci Ctr, Prote Core Facil, Tucson, AZ 85721 USA
关键词
Oxidative stress; Human diploid fibroblasts; Senescence; Gene expression; Proteomics; PROTEIN IDENTIFICATION TECHNOLOGY; INDUCED PREMATURE SENESCENCE; HYDROGEN-PEROXIDE; GENE-EXPRESSION; REPLICATIVE SENESCENCE; THIOREDOXIN REDUCTASE; TRANSCRIPTION FACTOR; MICROARRAY ANALYSIS; GROWTH ARREST; ANTIOXIDANT;
D O I
10.1007/s10522-008-9157-3
中图分类号
R592 [老年病学]; C [社会科学总论];
学科分类号
03 ; 0303 ; 100203 ;
摘要
A number of lines of evidence suggest that senescence of normal human diploid fibroblasts (HDFs) in culture is relevant to the process of aging in vivo. Using normal human skin diploid fibroblasts, we examine the changes in genes and proteins following treatment with a mild dose of H2O2, which induces premature senescence. Multidimensional Protein Identification Technology (MudPIT) in combination with mass spectrometry analyses of whole cell lysates from HDFs detected 65 proteins in control group, 48 proteins in H2O2-treated cells and 109 proteins common in both groups. In contrast, cDNA microarray analyses show 173 genes up-regulated and 179 genes down-regulated upon H2O2 treatment. Both MudPIT and cDNA microarray analyses indicate that H2O2 treatment caused elevated levels of thioredoxin reductase 1. Semi-quantitative RT-PCR and Western-blot were able to verify the finding. Out of a large number of genes or proteins detected, only a small fraction shows the overlap between the outcomes of microarray versus proteomics. The low overlap suggests the importance of considering proteins instead of transcripts when investigating the gene expression profile altered by oxidative stress.
引用
收藏
页码:125 / 151
页数:27
相关论文
共 51 条
[1]  
Andon NL, 2002, PROTEOMICS, V2, P1156, DOI 10.1002/1615-9861(200209)2:9<1156::AID-PROT1156>3.0.CO
[2]  
2-4
[3]   Regulation of metallothionein gene expression by oxidative stress and metal ions [J].
Andrews, GK .
BIOCHEMICAL PHARMACOLOGY, 2000, 59 (01) :95-104
[4]   Physiological functions of thioredoxin and thioredoxin reductase [J].
Arnér, ESJ ;
Holmgren, A .
EUROPEAN JOURNAL OF BIOCHEMISTRY, 2000, 267 (20) :6102-6109
[5]   Thioredoxin reductase as a pathophysiological factor and drug target [J].
Becker, K ;
Gromer, S ;
Schirmer, RH ;
Müller, S .
EUROPEAN JOURNAL OF BIOCHEMISTRY, 2000, 267 (20) :6118-6125
[6]  
Breci Linda, 2007, V355, P249
[7]   Fibroblasts regulate the switch from acute resolving to chronic persistent inflammation [J].
Buckley, CD ;
Pilling, D ;
Lord, JM ;
Akbar, AN ;
Scheel-Toellner, D ;
Salmon, M .
TRENDS IN IMMUNOLOGY, 2001, 22 (04) :199-204
[8]   Cellular senescence: when bad things happen to good cells [J].
Campisi, Judith ;
di Fagagna, Fabrizio d'Adda .
NATURE REVIEWS MOLECULAR CELL BIOLOGY, 2007, 8 (09) :729-740
[9]   Large scale protein profiling by combination of protein fractionation and multidimensional protein identification technology (MudPIT) [J].
Chen, EI ;
Hewel, J ;
Felding-Habermann, B ;
Yates, JR .
MOLECULAR & CELLULAR PROTEOMICS, 2006, 5 (01) :53-56
[10]   SENESCENCE-LIKE GROWTH ARREST INDUCED BY HYDROGEN-PEROXIDE IN HUMAN-DIPLOID FIBROBLAST F65 CELLS [J].
CHEN, Q ;
AMES, BN .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1994, 91 (10) :4130-4134