Construction of a human cardiovascular cDNA microarray: Portrait of the failing heart

被引:62
作者
Barrans, JD [1 ]
Stamatiou, D
Liew, CC
机构
[1] Harvard Univ, Brigham & Womens Hosp, Sch Med, Cardiovasc Genome Unit, Boston, MA 02115 USA
[2] Univ Toronto, Toronto Gen Hosp, Univ Hlth Network, Dept Lab Med & Pathobiol, Toronto, ON M5G 1L7, Canada
基金
英国医学研究理事会;
关键词
cDNA microarray; gene expression; heart failure;
D O I
10.1006/bbrc.2000.4137
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Identifying key genes that regulate the complex diseases of the cardiovascular system can be greatly facilitated with the use of microarrays. In an effort to obtain a global portrait of gene expression in the failing heart, we have constructed in-house a glass microscope slide cDNA microarray (termed "CardioChip") containing 10,368 redundant and randomly-selected sequenced expressed sequence tags (representing known genes, other matched ESTs, and novel, unmatched ESTs) derived from several human heart and artery cDNA libraries. From our preliminary data with Cy3- and Cy5-labeled probes, we have identified 38 transcripts showing a minimum twofold differential expression, among which are several novel or previously-uncharacterized genes. This array-representing what we believe to be the largest cardiovascular-based cDNA array to date-establishes a practical and invaluable platform for obtaining a global genetic portrait of complex cardiovascular diseases, particularly in the failing heart. (C) 2001 Academic Press.
引用
收藏
页码:964 / 969
页数:6
相关论文
共 28 条
[1]   The "final common pathway" hypothesis and inherited cardiovascular disease - The role of cytoskeletal proteins in dilated cardiomyopathy [J].
Bowles, NE ;
Bowles, KR ;
Towbin, JA .
HERZ, 2000, 25 (03) :168-175
[2]   Genomic circuits and the integrative biology of cardiac diseases [J].
Chien, KR .
NATURE, 2000, 407 (6801) :227-232
[3]   Desmin myopathy, a skeletal myopathy with cardiomyopathy caused by mutations in the desmin gene. [J].
Dalakas, MC ;
Park, KY ;
Semino-Mora, C ;
Lee, HS ;
Sivakumar, K ;
Goldfarb, LG .
NEW ENGLAND JOURNAL OF MEDICINE, 2000, 342 (11) :770-780
[4]   A cardiovascular EST repertoire: progress and promise for understanding cardiovascular disease [J].
Dempsey, AA ;
Ton, C ;
Liew, CC .
MOLECULAR MEDICINE TODAY, 2000, 6 (06) :231-237
[5]  
DeRisi J, 1996, NAT GENET, V14, P457
[6]   Expression profiling using cDNA microarrays [J].
Duggan, DJ ;
Bittner, M ;
Chen, YD ;
Meltzer, P ;
Trent, JM .
NATURE GENETICS, 1999, 21 (Suppl 1) :10-14
[7]   Altered regulatory properties of human cardiac troponin I mutants that cause hypertrophic cardiomyopathy [J].
Elliott, K ;
Watkins, H ;
Redwood, CS .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2000, 275 (29) :22069-22074
[8]   A MOLECULAR-BASIS FOR FAMILIAL HYPERTROPHIC CARDIOMYOPATHY - A BETA-CARDIAC MYOSIN HEAVY-CHAIN GENE MISSENSE MUTATION [J].
GEISTERFERLOWRANCE, AAT ;
KASS, S ;
TANIGAWA, G ;
VOSBERG, HP ;
MCKENNA, W ;
SEIDMAN, CE ;
SEIDMAN, JG .
CELL, 1990, 62 (05) :999-1006
[9]   A concise guide to cDNA microarray analysis [J].
Hegde, P ;
Qi, R ;
Abernathy, K ;
Gay, C ;
Dharap, S ;
Gaspard, R ;
Hughes, JE ;
Snesrud, E ;
Lee, N ;
Quackenbush, J .
BIOTECHNIQUES, 2000, 29 (03) :548-+
[10]   Increased expression of cytoskeletal, linkage, and extracellular proteins in failing human myocardium [J].
Heling, A ;
Zimmermann, R ;
Kostin, S ;
Maeno, Y ;
Hein, S ;
Devaux, B ;
Bauer, E ;
Klövekorn, WP ;
Schlepper, M ;
Schaper, W ;
Schaper, J .
CIRCULATION RESEARCH, 2000, 86 (08) :846-853