Isoproterenol-induced activation of MAPK, NFkappaB and JAK/STAT pathway in mouse myocardium.
- Author:
Feng YIN
1
;
Yun ZHU
;
Ping LI
;
Qi-De HAN
;
You-Yi ZHANG
Author Information
1. Institute of Vascular Medicine, Peking University Third Hospital, The Reference Laboratory of Education Ministry on Molecular Cardiology, Beijing 100083.
- Publication Type:Journal Article
- MeSH:
Animals;
Heart;
drug effects;
Isoproterenol;
pharmacology;
Janus Kinase 1;
metabolism;
Male;
Mice;
Mice, Inbred BALB C;
Mitogen-Activated Protein Kinases;
metabolism;
Myocardium;
metabolism;
NF-kappa B;
metabolism;
STAT3 Transcription Factor;
metabolism;
Signal Transduction;
Time Factors
- From:
Acta Physiologica Sinica
2003;55(4):449-453
- CountryChina
- Language:Chinese
-
Abstract:
This study was aimed to determine the in vivo signal transduction pathway responsible for isoproterenol (ISO)-induced cardiac hypertrophy or remodeling. Mice were treated with ISO (15 mg/kg body weight) or vehicle by intraperitoneal injection (i.p.). Activation of mitogen-activted protein kinase (MAPK), NF-kappaB and JAK/STAT pathway in the left ventricular myocardium was measured by Western blot analysis. ISO significantly activated MAPK (ERK1/2 and p38) at early phase (5 min); biphasic activation of NF-kappaB was observed in our in vivo study; and ISO caused a delayed STAT3 activation (at 60 to 240 min) in mouse myocardium. Taken together, these results indicate that ISO activates these signal transduction pathways in different time course.
