© 2000 by European Society of Cardiology
Copyright © 2000, European Society of Cardiology
Programmed cell death in the developing heart
aExperimental and Molecular Cardiology Group, Cardiovascular Research Institute Amsterdam, Academic Medical Center, Amsterdam, The Netherlands
bDepartment of Molecular Cell Biology and Genetics, Cardiovascular Research Institute Maastricht, University Maastricht, Maastricht, The Netherlands
cDepartment of Pathology Haynal University of Health Sciences, Budapest, Hungary
* Corresponding author. Tel.: +31-20-5669-111; fax: +31-20-6976-177 m.j.vandenhoff@amc.uva.nl a.f.moorman@amc.uva.nl
Received 29 July 1999; accepted 1 November 1999
KEYWORDS AIF, apoptosis-inducing factor; AP, aorticopulmonary; APAF, apoptotic protease activating factor; AVC, atrioventricular canal; CAD, caspase-activated Dnase; CARD, caspase recruitment domain; cIAP, cellular inhibitor of apoptosis; Daxx, death domain associated protein; DD, death domain; DED, death effecter domain; DM, dorsal mesocardium; DR, death receptor; DcR, decoy receptor; ED, embryonic day; ERK, extracellular signal-regulated kinases; FADD, Fas-associated death domain; FLIP, FADD-like interleukine-1 converting enzyme inhibitory proteins; H/H, Hamburger and Hamilton stage; IAS, interatrial septum; ICAD, inhibitor of caspase-activated DNase; IVS, interventricular septum; Jak/Stat, Janus kinase/signal transducer and activator of transcription; JNK, stress-activated c-Jun NH2-terminal kinase; LA, left atrium; LV, left ventricle; MAP, mammalian mitogen-activated protein; ND, neonatal day; NF-AT, nuclear factor of activated T-cells; OFT, outflow tract; PIF, primary interventricular foramen; PS, phosphatidylserine; RAIDD, RIP associated ICH1/CED3 homologous protein with death domain; RA, right atrium; RAR, retinoic acid receptors; RIP, receptor-interacting protein; RV, right ventricle; RxR, retinoidxreceptors; SODD, silencer of death domain; TNF, tumor necrosis factor; TNF-R, tumor necrosis factor receptor; TRADD, TNFR-associated death domain; TRAF, TNFR-associated factor; TUNEL, terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling
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1 Introduction |
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In humans every minute millions of cells die by programmed cell death and by the end of their life almost 99.9% of all cells once made have undergone this fate [1]. The functionality of cell death is different during development and adult life. During development apoptosis serves three major functions: deleting vestigial structures, i.e. phylogenetic cell death; controlling cell numbers, i.e. histogenetic cell death, and remodeling structures, i.e. morphogenetic cell death [2]. In adult life, apoptosis mainly serves to maintain homeostasis by counterbalancing mitosis and deleting cells, which are potentially autoimmunoreactive, malignant, or virus infected [3,4].
In contrast to adult life cell death, where cell death is generally considered a pathological event, during cardiac development cell death is a physiological event that is highly regulated in space and time. It took till 1968 when cell death was first recognized in the chicken ventricular myocardium [5]. In
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2 Detection of cell death |
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2.1 Morphological methods
2.1.1 Histological analysis
2.1.2 Histochemical analysis
2.1.3 Supravital staining procedures
2.1.4 Ultrastructural analysis
2.2 Biochemical and/or molecular methods
2.2.1 Detection of apoptosis-associated DNA fragmentation
2.2.2 Exposure of phosphatidylserine on the plasma membrane
2.2.3 Detection of apoptosis-associated antigens
2.3 Concluding remarks
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3 Spatiotemporal distribution of cell death in the developing heart |
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3.1 Spatiotemporal pattern of apoptosis in the developing chicken heart based on morphological studies (Fig. 2)
3.2 Spatiotemporal pattern of apoptosis in the developing chicken heart based on molecular studies
3.3 Interspecies differences in the zones of cell death
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4 Teratogens, zones of cell death and cardiac malformations |
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5 The molecular mechanism of apoptosis in the developing heart |
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5.1 Alteration of the membrane composition (Fig. 4)
5.2 Death receptor mediated signalling (Fig. 4)
5.3 Cell death mediated via the mitochondria (Fig. 4)
5.4 Growth factor withdrawal induced cell death
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6 Concluding remarks and future perspective |
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