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Regulation of Embryonic Cardiac Wall Growth and Vascularization by FGF‐2
Author(s) -
Nanka Ondrej,
Petrovova Elena,
Fikrle Michal,
deAlmeida Angela,
Sedmera David
Publication year - 2009
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.23.1_supplement.642.3
Subject(s) - fibroblast growth factor , paracrine signalling , embryonic stem cell , myocyte , biology , embryonic heart , cell growth , medicine , cardiac myocyte , endocrinology , microbiology and biotechnology , receptor , gene , genetics
The aim of this study was to assess the effect of FGF‐2 signaling on growth of chick embryonic ventricular wall and its vascularization. In the first set of experiments, left ventricular wall of embryonic day 7 (E7) chick embryos was injected with either GFP‐expressing replication‐deficient adenovirus alone or in combination with adenoviral vector encoding human FGF‐2 gene. In the second set of experiments, FGF signaling was blocked in E8 embryos using FGFR1 receptor tyrosine kinase inhibitor SU 5402. Cell proliferation was measured in both cases using BrdU incorporation and immunohistochemistry on E9. Morphological examination of adenovirus‐injected hearts revealed no difference in normal myocardial architecture, but increased levels of myocyte proliferation in hearts injected with FGF‐2 adenovirus. There was no difference in capillary density or coronary artery anomalies. Blocking of FGF signaling with SU 5402 led to hemorrhages in the areas of developing vasculature in the tips of limbs and epicardium. However, the rate of myocyte proliferation was unchanged. We conclude that up‐regulation of FGF‐2 signaling has a positive effect on growth of the early fetal heart, while its inhibition impacts mainly vasculogenesis, pointing to functional redundancy in paracrine control of myocyte proliferation in the developing heart. Supported by MSMT VZ 0021620806, LC 06061, AS CR AVOZ50450515. Grant Funding Source MSMT VZ 0021620806