Role of the Wilms' tumour transcription factor, Wt1, in blood vessel formation

被引:17
作者
Scholz, Holger [1 ]
Wagner, Kay-Dietrich [2 ,3 ]
Wagner, Nicole [2 ,3 ]
机构
[1] Charite Univ Med Berlin, Inst Vegetat Physiol, D-10117 Berlin, Germany
[2] Fac Med Nice, INSERM, U907, F-06034 Nice, France
[3] Univ Nice Sophia Antipolis, Fac Med, Nice, France
来源
PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY | 2009年 / 458卷 / 02期
关键词
Wilms' tumour suppressor Wt1; Heart development; Cardiac ischaemia; Tumor angiogenesis; SMOOTH-MUSCLE-CELLS; SUPPRESSOR GENE WT1; INDUCIBLE FACTOR-I; GROWTH-FACTOR; FACTOR ETS-1; EXPRESSION; HYPOXIA; ANGIOGENESIS; EPICARDIUM; PROTEIN;
D O I
10.1007/s00424-008-0621-3
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
Blood vessel formation is important for normal organ development and tumour growth. A highly specialised developmental program of vessel formation exists in the heart and is essential for normal cardiogenesis. From mouse models, it became clear that the Wilms' tumour protein Wt1 is required for normal heart development. Originally identified as a tumour suppressor gene based on its mutational inactivation in Wilms' tumour or nephroblastoma, Wt1 is nowadays recognised to have much broader functions in organogenesis and pathophysiology. The multiple tasks of Wt1 are not only limited to the kidney but involve the heart and vascular system as well. In this review, we focus on recent findings about the importance of Wt1 in heart and coronary vessel development and the identified molecular mechanisms. In addition, we discuss the implication of Wt1 in the vascular response to myocardial ischaemia and its oncogenic potential as a promoter of tumour angiogenesis.
引用
收藏
页码:315 / 323
页数:9
相关论文
共 90 条
[11]   Development of an siRNA-based method for repressing specific genes in renal organ culture and its use to show that the Wt1 tumour suppressor is required for nephron differentiation [J].
Davies, JA ;
Ladomery, M ;
Hohenstein, P ;
Michael, L ;
Shafe, A ;
Spraggon, L ;
Hastie, N .
HUMAN MOLECULAR GENETICS, 2004, 13 (02) :235-246
[12]   Molecular interactions between neurotrophin receptors [J].
Dechant, G .
CELL AND TISSUE RESEARCH, 2001, 305 (02) :229-238
[13]   Common epicardial origin of coronary vascular smooth muscle, perivascular fibroblasts, and intermyocardial fibroblasts in the avian heart [J].
Dettman, RW ;
Denetclaw, W ;
Ordahl, CP ;
Bristow, J .
DEVELOPMENTAL BIOLOGY, 1998, 193 (02) :169-181
[14]  
Donovan MJ, 2000, DEVELOPMENT, V127, P4531
[15]  
Duband JL, 1995, ACTA ANAT, V154, P63
[16]   Heterozygous embryonic lethality induced by targeted inactivation of the VEGF gene [J].
Ferrara, N ;
CarverMoore, K ;
Chen, H ;
Dowd, M ;
Lu, L ;
OShea, KS ;
PowellBraxton, L ;
Hillan, KJ ;
Moore, MW .
NATURE, 1996, 380 (6573) :439-442
[17]  
Fischer C, 2006, Handb Exp Pharmacol, P157
[18]   Angioblast-mesenchyme induction of early kidney development is mediated by Wt1 and Vegfa [J].
Gao, XB ;
Chen, X ;
Taglienti, M ;
Rumballe, B ;
Little, MH ;
Kreidberg, JA .
DEVELOPMENT, 2005, 132 (24) :5437-5449
[19]   Epicardium-derived cells contribute a novel population to the myocardial wall and the atrioventricular cushions [J].
Gittenberger-de Groot, AC ;
Peeters, MPFMV ;
Mentink, MMT ;
Gourdie, RG ;
Poelmann, RE .
CIRCULATION RESEARCH, 1998, 82 (10) :1043-1052
[20]   ALTERNATIVE SPLICING AND GENOMIC STRUCTURE OF THE WILMS-TUMOR GENE-WT1 [J].
HABER, DA ;
SOHN, RL ;
BUCKLER, AJ ;
PELLETIER, J ;
CALL, KM ;
HOUSMAN, DE .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1991, 88 (21) :9618-9622