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Computational Analyses of Endocardial Cell Motion During Cardiovascular Morphogenesis in Transgenic Avian Embryos
Author(s) -
Aleksandrova Anastasiia,
Czirok Andras,
Lansford Rusty D,
Szabo Andras,
Little Charles D,
Rongish Brenda J
Publication year - 2010
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.24.1_supplement.180.3
Subject(s) - extracellular matrix , microbiology and biotechnology , biology , morphogenesis , motility , progenitor cell , live cell imaging , fibronectin , anatomy , stem cell , cell , biochemistry , gene
Conventional dogma suggests that cardiac progenitors migrate to the midline to form a tubular heart, comprised of concentric myocardial and endocardial layers separated by extracellular matrix (ECM). Here we describe the motility of fluorescently tagged (Tie1‐YFP) endocardial progenitors in transgenic quail embryos using epifluorescent time lapse imaging. To visualize the extracellular matrix environment of migrating progenitor cells, we labeled fibronectin and fibrillin‐2 in vivo by microinjection of fluorochrome‐conjugated monoclonal antibodies. Imaging was performed at early stages, encompassing tubular heart assembly and early looping. We determined the relative importance of directed cell autonomous motility versus passive tissue movements in the assembly of a tubular heart. We established the motion of cells and fibrils of multiple ECM components using both object tracking and particle image velocimetry (image cross correlation). These quantitative data indicate the contribution of cell autonomous motility displayed by endocardial progenitors is limited. Thus tissue‐level motion drives most of the cell displacements during endocardial morphogenesis. Studies using motility inhibitors and Tie1+ cell transplantation will assess the role of myosin II‐dependent directed endocardial progenitor cell migration in early stages of tubular heart morphogenesis. Supported by NIH HL085694. Grant Funding Source : NIH HL085694