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FGF signaling is involved in physiological adaptation to pressure overload in developing heart
Author(s) -
Krejci Eliska,
Pesevski Zivorad,
Nanka Ondrej,
Sedmera David
Publication year - 2012
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.26.1_supplement.15.1
Subject(s) - pressure overload , myocyte , blot , fibroblast growth factor , medicine , embryonic stem cell , paracrine signalling , endocrinology , bromodeoxyuridine , biology , immunohistochemistry , microbiology and biotechnology , andrology , muscle hypertrophy , biochemistry , cardiac hypertrophy , receptor , gene
Fibroblast growth factors (FGFs) play an important role during embryonic induction, growth and patterning. Exogenous FGF2 as well as pressure loading were shown to induce embryonic myocyte proliferation. Here we tested whether FGF2 signaling is involved in transmission of pressure overload to increased myocyte proliferation in vivo. Pressure overload was induced by conotruncus constriction in Stage 21 chick embryos. Anti‐bromodeoxyuridine labeling was used to assess proliferation at 24, 48 and 72 h. Western blotting and RT‐PCR to measure FGF2 protein and mRNA levels was performed on ventricular extracts at 48 h interval. Blood was collected at 48 h to assess the amount of FGF2 in serum by ELISA. Proliferation of ventricular myocytes was increased significantly at 48 h. Neither western blotting, nor immunohistochemistry revealed any changes in the amount of myocardial FGF2. ELISA showed a 93% increase of FGF2 in the serum. Increased amount of FGF2 mRNA in ventricular myocardium was confirmed by real time PCR. We conclude that FGF2 synthesis is increased in embryonic ventricular cardiomyocytes in response to increased stretch due to pressure overload. Increased stretch causes its release into serum, causing it to act in endocrine, rather then paracrine manner. Supported by Ministry of Education VZ 0021620806, ASCR AV0Z50450515 and AV0Z50110509 and GACR P302/11/1308. Grant Funding Source : P302/11/1308