Differential roles of MAPKs and MSK1 signalling pathways in the regulation of c-Jun during phenylephrine-induced cardiac myocyte hypertrophy

Επιστημονική δημοσίευση - Άρθρο Περιοδικού uoadl:3090285 9 Αναγνώσεις

Μονάδα:
Ερευνητικό υλικό ΕΚΠΑ
Τίτλος:
Differential roles of MAPKs and MSK1 signalling pathways in the regulation of c-Jun during phenylephrine-induced cardiac myocyte hypertrophy
Γλώσσες Τεκμηρίου:
Αγγλικά
Περίληψη:
Gq-protein-coupled receptor (GqPCR) signalling is associated with the induction of cardiac myocyte hypertrophy, which is characterized by an increase in expression of immediate early genes via activation of pre-existing transcription factors. Here, we explore the role of MSK1 and MAPK signalling pathways in the regulation of the immediate early gene c-jun. The results provide further support for the role of MSK1 in cardiac myocyte hypertrophy and indicate that PE activates distinct signalling mechanisms which culminate with a complex activation of c-jun. ERK1/2 and JNKs are the principal kinases responsible for phosphorylation of c-Jun, whereas c-jun mRNA and protein up-regulation by PE is mediated by multiple signalling pathways that include MSK1, ERK1/2, p38-MAPK and JNKs. These signalling mechanisms seem to be critical to the phenotypic changes of cardiac myocytes in response to hypertrophic stimulation. © Springer Science+Business Media, LLC. 2008.
Έτος δημοσίευσης:
2009
Συγγραφείς:
Markou, T.
Cieslak, D.
Gaitanaki, C.
Lazou, A.
Περιοδικό:
Molecular and Cellular Biochemistry
Τόμος:
322
Αριθμός / τεύχος:
1-2
Σελίδες:
103-112
Λέξεις-κλειδιά:
messenger RNA; mitogen activated protein kinase; mitogen activated protein kinase 3; phenylephrine; protein c jun; stress activated protein kinase; stress activated protein kinase 1; synaptophysin, animal cell; animal experiment; animal model; article; cell activation; cell stimulation; controlled study; gene activation; gene control; gene function; gene interaction; heart muscle cell; heart ventricle hypertrophy; male; nonhuman; nucleotide sequence; pathogenesis; protein phosphorylation; rat; signal transduction; upregulation, Animals; Cardiomegaly; Cell Enlargement; JNK Mitogen-Activated Protein Kinases; Male; MAP Kinase Signaling System; Mitogen-Activated Protein Kinase 1; Mitogen-Activated Protein Kinase 3; Mitogen-Activated Protein Kinases; Myocytes, Cardiac; Phenylephrine; Phosphorylation; Proto-Oncogene Proteins c-jun; Rats; Ribosomal Protein S6 Kinases, 90-kDa; RNA, Messenger; Up-Regulation
Επίσημο URL (Εκδότης):
DOI:
10.1007/s11010-008-9945-8
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