[Isoproterenol-induced activation of MAPK, NFkappaB and JAK/STAT pathway in mouse myocardium].
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.
Yin
Feng
F
Institute of Vascular Medicine, Peking University Third Hospital, The Reference Laboratory of Education Ministry on Molecular Cardiology, Beijing 100083.
Zhu
Yun
Y
Li
Ping
P
Han
Qi-De
QD
Zhang
You-Yi
YY
D000818:Animals; D006321:Heart / Q000187:drug effects; D007545:Isoproterenol / Q000494:pharmacology*; D053613:Janus Kinase 1 / Q000378:metabolism; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D020928:Mitogen-Activated Protein Kinases / Q000378:metabolism*; D009206:Myocardium / Q000378:metabolism*; D016328:NF-kappa B / Q000378:metabolism*; D050796:STAT3 Transcription Factor / Q000378:metabolism; D015398:Signal Transduction; D013997:Time Factors
D016328:NF-kappa B; D050796:STAT3 Transcription Factor; D053613:Janus Kinase 1; D020928:Mitogen-Activated Protein Kinases; D007545:Isoproterenol