[Isoproterenol-induced activation of MAPK, NFkappaB and JAK/STAT pathway in mouse myocardium]

Sheng Li Xue Bao. 2003 Aug 25;55(4):449-53.
[Article in 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.

Publication types

  • English Abstract
  • Research Support, Non-U.S. Gov't

MeSH terms

  • 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

Substances

  • NF-kappa B
  • STAT3 Transcription Factor
  • Janus Kinase 1
  • Mitogen-Activated Protein Kinases
  • Isoproterenol