TY - JOUR
TI - Differential roles of MAPKs and MSK1 signalling pathways in the regulation of c-Jun during phenylephrine-induced cardiac myocyte hypertrophy
AU - Markou, T.
AU - Cieslak, D.
AU - Gaitanaki, C.
AU - Lazou, A.
JO - Molecular and Cellular Biochemistry
PY - 2009
VL - 322
TODO - 1-2
SP - 103-112
PB - 
SN - 0300-8177
TODO - 10.1007/s11010-008-9945-8
TODO - 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
TODO - 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.
ER -