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Cell death in the atrioventricular canal myocardium determines ventricular activation patterns
Author(s) -
Nanka Ondrej,
Grim Milos,
Sedmera David
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.lb14
Subject(s) - apex (geometry) , apoptosis , optical mapping , embryonic stem cell , programmed cell death , atrioventricular canal , immunostaining , anatomy , microbiology and biotechnology , biology , medicine , chemistry , heart disease , immunohistochemistry , biochemistry , gene
We hypothesize that apoptosis in the AV myocardium influences maturation of atrioventricular conduction axis. We thus blocked apoptosis in chick embryonic heart and analyzed the effects of this treatment on cell death and ventricular activation patterns. ED4 chick embryos were treated with the caspase inhibitor zVAD by intrapericardial injection. Spontaneously beating hearts isolated at ED8 were stained with voltage‐sensitive dye and imaged with a high‐speed camera. Amount of apoptotic cells was analyzed at ED 7 by whole mount LysoTracker Red or active caspase immunostaining and confocal microscopy. Hearts of embryos treated with zVAD showed a significantly increased proportion of immature (base to apex) activation patterns at ED8, including ventricular activation originating from right AV junction, a pattern never observed in control hearts. The number of apoptotic cells in AV canal myocardium was decreased at ED7 in the treated hearts. Apoptosis in the AV canal myocardium is thus an important contributor to activation pattern development. Its inhibition at critical stages can lead to persistence of accessory AV connections, which form a morphological substrate for ventricular pre‐excitation. Supported by project of MSMT VZ 0021620806, LC 06061.