Activation of mitogen-activated protein kinases in the non-ischemic myocardium of an acute myocardial infarction in rats
Citation
K. Yoshida et al., Activation of mitogen-activated protein kinases in the non-ischemic myocardium of an acute myocardial infarction in rats, JPN CIRC J, 65(9), 2001, pp. 808-814
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
JAPANESE CIRCULATION JOURNAL-ENGLISH EDITION
SICI code
0047-1828(200109)65:9<808:AOMPKI>2.0.ZU;2-F
Abstract
As one of the signal transduction pathways related to myocardial remodeling
, mitogen-activated protein kinases (MAPKs) possibly play an important role
in ischemic heart disease, but it is still unknown whether myocardial MAPK
s are activated in the non-ischemic region of an acute myocardial infarctio
n (AMI). Therefore, the present study investigated the myocardial activity
of extracellular signal-regulated kinases (ERKs), c-Jun NH2 terminal kinase
s (JNKs) and p38MAPK during the acute phase of an infarction of the rat hea
rt, and measured the geometrical ventricular changes by echocardiography. A
ll MAPKs were significantly activated in the ischemic myocardium (IM), non-
ischemic septal wall (SW), and right ventricular wall (RV). Furthermore, th
e activation patterns of MAPKs differed in each region. The activation of p
44ERK, JNKs and p38MAPK in the IM occurred rapidly after myocardial ischemi
a, followed by those in the SW and RV. The activator protein-1 DNA binding
activities of the IM, SW and RV increased significantly at 1 day after coro
nary ligation. Echocardiography showed increased SW motion and RV dilatatio
n. In conclusion, this is the first in vivo evidence that myocardial MAPKs
are activated in the non-ischemic region of an AMI. Echocardiographic resul
ts suggest that acceleration of workload and/or stretch may partially induc
e the activation of MAPKs.