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Apoptosis and epicardial contributions act as complementary factors in remodeling of the atrioventricular canal myocardium and atrioventricular conduction patterns in the embryonic chick heart
R. Vicente Steijn, D. Sedmera, NA. Blom, M. Jongbloed, A. Kvasilova, O. Nanka,
Language English Country United States
Document type Journal Article, Research Support, Non-U.S. Gov't
NLK
Free Medical Journals
from 1992 to 1 year ago
Medline Complete (EBSCOhost)
from 2012-07-01 to 1 year ago
Wiley Free Content
from 1996 to 1 year ago
PubMed
30152577
DOI
10.1002/dvdy.24642
Knihovny.cz E-resources
- MeSH
- Epithelial Cell Adhesion Molecule MeSH
- Apoptosis * MeSH
- Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels MeSH
- Chick Embryo MeSH
- Pericardium * MeSH
- Pre-Excitation Syndromes etiology MeSH
- Heart Conduction System physiopathology MeSH
- Ventricular Remodeling * MeSH
- Atrial Remodeling * MeSH
- Animals MeSH
- Check Tag
- Chick Embryo MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
BACKGROUND: During heart development, it has been hypothesized that apoptosis of atrioventricular canal myocardium and replacement by fibrous tissue derived from the epicardium are imperative to develop a mature atrioventricular conduction. To test this, apoptosis was blocked using an established caspase inhibitor and epicardial growth was delayed using the experimental epicardial inhibition model, both in chick embryonic hearts. RESULTS: Chicken embryonic hearts were either treated with the peptide caspase inhibitor zVAD-fmk by intrapericardial injection in ovo (ED4) or underwent epicardial inhibition (ED2.5). Spontaneously beating embryonic hearts isolated (ED7-ED8) were then stained with voltage-sensitive dye Di-4-ANEPPS and imaged at 0.5-1 kHz. Apoptotic cells were quantified (ED5-ED7) by whole-mount LysoTracker Red and anti-active caspase 3 staining. zVAD-treated hearts showed a significantly increased proportion of immature (base to apex) activation patterns at ED8, including ventricular activation originating from the right atrioventricular junction, a pattern never observed in control hearts. zVAD-treated hearts showed decreased numbers of apoptotic cells in the atrioventricular canal myocardium at ED7. Hearts with delayed epicardial outgrowth showed also increased immature activation patterns at ED7.5 and ED8.5. However, the ventricular activation always originated from the left atrioventricular junction. Histological examination showed no changes in apoptosis rates, but a diminished presence of atrioventricular sulcus tissue compared with controls. CONCLUSIONS: Apoptosis in the atrioventricular canal myocardium and controlled replacement of this myocardium by epicardially derived HCN4-/Trop1- sulcus tissue are essential determinants of mature ventricular activation pattern. Disruption can lead to persistence of accessory atrioventricular connections, forming a morphological substrate for ventricular pre-excitation. Developmental Dynamics 247:1033-1042, 2018. © 2018 Wiley Periodicals, Inc.
Department of Pediatric Cardiology Leiden University Medical Center Leiden The Netherlands
Institute of Anatomy 1st Faculty of Medicine Charles University Prague Czech Republic
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