Notch signalling in ventricular chamber development and cardiomyopathy

被引:59
作者
D'Amato, Gaetano [1 ]
Luxan, Guillermo [1 ,2 ]
Luis de la Pompa, Jose [1 ]
机构
[1] Ctr Nacl Invest Cardiovasc Carlos III CNIC, Intercellular Signalling Cardiovasc Dev & Dis Lab, Melchor Fernandez Almagro 3, E-28029 Madrid, Spain
[2] Max Planck Inst Mol Biomed, Dept Tissue Morphogenesis, Rontgenstr 20, D-48149 Munster, Germany
关键词
cardiomyopathy; compaction; heart; left ventricular noncompaction; NOTCH; signalling; trabeculae; ventricles; CARDIAC CONDUCTION SYSTEM; EMBRYONIC MOUSE HEART; CORONARY-ARTERIES; NON-COMPACTION; MIND BOMB; ISOLATED NONCOMPACTION; INTRACELLULAR DOMAIN; TRANSCRIPTION FACTOR; NEUREGULIN RECEPTOR; ENDOTHELIAL-CELLS;
D O I
10.1111/febs.13773
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
The vertebrate heart is the first organ to form and function during embryogenesis. Primitive streak-derived cardiac progenitors located bilaterally move rostral to form the primitive heart tube that subsequently undergoes rightward looping, remodelling and septation to give rise to the mature four-chambered heart. Tightly regulated tissue interactions orchestrate the patterning, proliferation and differentiation processes that give rise to the adult ventricles. Studies in animal models have demonstrated the crucial function of the Notch signalling pathway in ventricular development and how alterations in human NOTCH signalling may lead to disease in the form of cardiomyopathies, such as left ventricular noncompaction (LVNC). In this review, we discuss how during trabecular formation and ventricular compaction, Dll4-Notch1 signals from chamber endocardium to regulate cardiomyocyte proliferation and differentiation in a noncell autonomous fashion and how, at later stages, myocardial Jag1 and Jag2 activate Notch1 in chamber endocardium to sustain chamber patterning and compaction with simultaneous coronary vessel development mediated by Dll4-Notch1. We suggest that alterations in these molecular mechanisms underlie MIB1-related familial LVNC and favour the hypothesis that this cardiomyopathy has a congenital nature.
引用
收藏
页码:4223 / 4237
页数:15
相关论文
共 101 条
[1]  
[Anonymous], HEART
[2]  
[Anonymous], 2007, Semin Cell Dev Biol
[3]   Mind bomb1 is a ubiquitin ligase essential for mouse embryonic development and Notch signaling [J].
Barsi, JC ;
Rajendra, R ;
Wu, JI ;
Artzt, K .
MECHANISMS OF DEVELOPMENT, 2005, 122 (10) :1106-1117
[4]  
BETTENHAUSEN B, 1995, DEVELOPMENT, V121, P2407
[5]   A novel X-linked gene, G4.5. is responsible for Barth syndrome [J].
Bione, S ;
DAdamo, P ;
Maestrini, E ;
Gedeon, AK ;
Bolhuis, PA ;
Toniolo, D .
NATURE GENETICS, 1996, 12 (04) :385-389
[6]   The Adhesion GPCRs:: A unique family of G protein-coupled receptors with important roles in both central and peripheral tissues [J].
Bjarnadottir, T. K. ;
Fredriksson, R. ;
Schioth, H. B. .
CELLULAR AND MOLECULAR LIFE SCIENCES, 2007, 64 (16) :2104-2119
[7]   Intracellular cleavage of notch leads to a heterodimeric receptor on the plasma membrane [J].
Blaumueller, CM ;
Qi, HL ;
Zagouras, P ;
ArtavanisTsakonas, S .
CELL, 1997, 90 (02) :281-291
[8]   A novel proteolytic cleavage involved in Notch signaling:: The role of the disintegrin-metalloprotease TACE [J].
Brou, C ;
Logeat, F ;
Gupta, N ;
Bessia, C ;
LeBail, O ;
Doedens, JR ;
Cumano, A ;
Roux, P ;
Black, RA ;
Israël, A .
MOLECULAR CELL, 2000, 5 (02) :207-216
[9]   Building the mammalian heart from two sources of myocardial cells [J].
Buckingham, M ;
Meilhac, S ;
Zaffran, S .
NATURE REVIEWS GENETICS, 2005, 6 (11) :826-835
[10]   Left ventricular non-compaction: Genetic heterogeneity, diagnosis and clinical course [J].
Captur, Gabriella ;
Nihoyannopoulos, Petros .
INTERNATIONAL JOURNAL OF CARDIOLOGY, 2010, 140 (02) :145-153