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IGF‐1 induces proliferation and T 3 causes maturation of cultured embryonic chicken cardiomyocytes
Author(s) -
SvenssonHolm AnnCharlotte B,
Lindgren Isa,
Österman Hanna,
Altimiras Jordi
Publication year - 2013
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.27.1_supplement.1187.7
Subject(s) - dapi , biology , cell growth , muscle hypertrophy , endocrinology , hyperplasia , myocyte , medicine , embryonic stem cell , microbiology and biotechnology , andrology , staining , genetics , gene
Fetal cardiac growth in mammalian models occurs primarily by cell proliferation (hyperplasia). However, close to term most cardiomyocytes lose the ability to proliferate and heart growth continues by increase in cell size (hypertrophy). The thyroid hormone T 3 is an important driver of this process. In contrast, chicken cardiomyocytes keep their proliferating ability long after hatching but little information is available on the mechanisms controlling cell growth and myocyte maturation in the chicken heart. Our aim was to study the effect of T 3 , IGF‐1 and Ang‐II on the proliferation and growth of embryonic chicken cardiomyocytes (ECCM), enzymatically isolated from E19 chicken embryos. Hyperplasia was measured using a proliferation assay (MTS) and hypertrophy/maturation was analysed morphologically by phalloidin staining of F‐actin and nuclear staining with DAPI. We show that IGF‐1 induces a significant increase in ECCM proliferation (30%) which is absent with T 3 or Ang‐II. The thyroid hormone T 3 caused multinucleation while none of the treatments had any hypertrophic effect. In conclusion, our results are similar to those obtained in sheep cardiomyocytes and show that ECCM proliferation is mediated through mechanisms involving IGF‐1 while T 3 causes maturation. Supported by FORMAS Centre of Excellence in Animal Welfare Science and career grant from Linköpings universitet to JA.