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Growth Dynamics and Mononucleation of the Ventricular Conduction System
Author(s) -
Sedmera David,
Gourdie Robert
Publication year - 2015
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.29.1_supplement.557.2
Subject(s) - myocyte , biology , embryonic stem cell , anatomy , confocal microscopy , microbiology and biotechnology , andrology , medicine , biochemistry , gene
During embryonic development, mammalian myocyte size does not change significantly. The switch from hyperplastic to hypertrophic growth occurs during the neonatal period. All previous studies have focused on working myocytes, which form 99% of ventricular mass; little is known about developmental changes in cell size, shape, and nucleation of cells of the ventricular conduction system (VCS). Hearts from Cx40:GFP transgenic mice were sampled at embryonic day 14, postnatal day 10, and adulthood (6 months). The ventricles were dissected, nuclei stained whole mount with Hoechst 33342, and specimens cleared in Scale/2 and flat mounted for confocal microscopy. Z‐series were acquired using a 40x oil immersion lens spanning at least 50 mm. Cell dimensions, nuclear count and volumes were measured separately for working and VCS myocytes. At the embryonic stage, green (Cx40‐expressing VCS cells) were larger than negative myocytes. This difference was reversed at postnatal day 10, where there was also differences in size between left bundle branch cells and Purkinje myocytes. The difference in cell volume was most pronounced at the adult stage. The transverse diameter was significantly smaller in adult VCS cells, giving them more elongated shape. Binucleated VCS cells were observed only rarely (<5%) during embryonic and neonatal stages; none (0/82) were seen in the adult. In conclusion, we show that the VCS in mouse is formed by a morphometrically distinct mononucleated cells with shape and size significantly different from working myocytes Supported by AAA travel grant and GACR P302/11/1308 and 13‐12412S.