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ERK, p38 and JNK MAPK are differently distributed and activated in the anoxic‐reogygenated embryonic heart
Author(s) -
Gardier Stephany,
Pedretti Sarah,
Sarre Alexandre,
Raddatz Eric
Publication year - 2008
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.22.1_supplement.750.14
Subject(s) - mapk/erk pathway , p38 mitogen activated protein kinases , phosphorylation , kinase , mitogen activated protein kinase , hypoxia (environmental) , microbiology and biotechnology , chemistry , protein kinase a , biology , medicine , oxygen , organic chemistry
Involvement of Mitogen Activated Protein Kinases (MAPK) ERK, p38 and JNK in the response of the developing heart to anoxia‐reoxygenation is not known. In an embryonic heart model we sought to determine the activation of MAPKs in atria (A), ventricle (V) and outflow tract (OT) during anoxia‐reoxygenation and after a severe oxidative stress. Content of MAPKs and their profile of activation during 30 min of anoxia and 60 min of reoxygenation were assessed by western immunoblotting and kinase assay in A, V and OT of hearts isolated from 4‐day‐old chick embryos. MAPKs phosphorylation was also determined after exposure to H 2 O 2 (1mM, 1h). Basal total and phosphorylated forms of ERK, p38 and JNK were the highest in V. Phosphorylation of ERK decreased twofold in A during anoxia, that of p38 increased twofold in A and V and returned to basal level at the end of reoxygenation. In OT, phosphorylation of ERK and p38 was not detectable. JNK activity peaked fivefold only in V after 30 min of reoxygenation. Exogenous H 2 O 2 increased ERK and p38 phosphorylation more markedly in A and OT, with no effect on JNK. Thus, in the embryonic heart ERK, p38 and JNK are differently distributed and modulated by anoxia‐reoxygenation and oxyradicals. Such findings provide a first step in understanding modulation of the MAPK cascades in the fetal heart subjected to intrauterine hypoxia. Supported by the Swiss National Science Foundation n°3100A0‐105901