Gene expression in pediatric heart disease with emphasis on conotruncal defects

被引:7
作者
Bittel, Douglas C. [1 ,2 ]
Kibiryeva, Nataliya [1 ,2 ]
O'Brien, James E. [2 ,3 ]
Lofland, Gary K. [2 ,3 ]
Butler, Merlin G. [1 ,2 ]
机构
[1] Childrens Mercy Hosp & Clin, Sect Med Genet & Mol Med, 2401 Gillham Rd, Kansas City, MO 64108 USA
[2] Univ Missouri, Kansas City Sch Med, Kansas City, MO 64108 USA
[3] Childrens Mercy Hosp & Clin, Sect Cardiovasc & Thorac Surg, Kansas City, MO USA
关键词
Congenital heart defects; Pediatric cardiology; Gene expression; Microarray; Conotruncal defects; Cardiac development;
D O I
10.1016/j.ppedcard.2005.04.004
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Developmental abnormalities of the heart are the underlying cause of many congenital heart malformations. The embryological development of the integrated cardiovascular tissue is the result of multiple tissue and cell-to-cell interactions involving temporal and spatial events under genetic control. Recent technological advances, like microarray analysis of gene expression, are providing new tools to aid in deciphering the complex networks of gene expression that regulate cardiac development. Here, we review our current understanding of the genetics of congenital heart disorders with emphasis on gene expression studies and report preliminary data from infants with conotruncal defects. We report our microarray analysis showing over-and underexpression of individual genes and gene network interactions from dysplastic pulmonic tissue from two infants with tetralogy of Fallot compared with normal pulmonic tissue from an unaffected control infant. (C) 2005 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:127 / 141
页数:15
相关论文
共 49 条
[1]   Construction of a human cardiovascular cDNA microarray: Portrait of the failing heart [J].
Barrans, JD ;
Stamatiou, D ;
Liew, CC .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 2001, 280 (04) :964-969
[2]   Monitoring of the subtraction process in solid-phase representational difference analysis:: characterization of a candidate drug [J].
Boräng, S ;
Andersson, T ;
Thelin, A ;
Larsson, M ;
Odeberg, J ;
Lundeberg, J .
GENE, 2001, 271 (02) :183-192
[3]  
Clark E.B., 1986, GENETICS CARDIOVASCU, P3
[4]   Pathogenetic mechanisms of congenital cardiovascular malformations revisited [J].
Clark, EB .
SEMINARS IN PERINATOLOGY, 1996, 20 (06) :465-472
[5]   Cardiovascular genomics: Estimating the total number of genes expressed in the human cardiovascular system [J].
Dempsey, AA ;
Dzau, VJ ;
Liew, CC .
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 2001, 33 (10) :1879-1886
[6]   Tetralogy of Fallot and other congenital heart defects in Hey2 mutant mice [J].
Donovan, J ;
Kordylewska, A ;
Jan, YN ;
Utset, MF .
CURRENT BIOLOGY, 2002, 12 (18) :1605-1610
[7]  
Ferencz C, 1997, GENETIC ENV RISK FAC
[8]  
Fujiwara T, 2002, DEVELOPMENT, V129, P4685
[9]   Tbx1, a DiGeorge syndrome candidate gene, is regulated by Sonic hedgehog during pharyngeal arch development [J].
Garg, V ;
Yamagishi, C ;
Hu, TH ;
Kathiriya, IS ;
Yamagishi, H ;
Srivastava, D .
DEVELOPMENTAL BIOLOGY, 2001, 235 (01) :62-73
[10]   Characterization of the TBX5 binding site and analysis of mutations that cause Holt-Oram syndrome [J].
Ghosh, TK ;
Packham, EA ;
Bonser, AJ ;
Robinson, TE ;
Cross, SJ ;
Brook, JD .
HUMAN MOLECULAR GENETICS, 2001, 10 (18) :1983-1994