Activation of gp130 Transduces Hypertrophic Signals via STAT3 in Cardiac Myocytes
Author(s) -
Keita Kunisada,
Eiroh Tone,
Yasushi Fujio,
Hideo Matsui,
Keiko YamauchiTakihara,
Tadamitsu Kishimoto
Publication year - 1998
Publication title -
circulation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.795
H-Index - 607
eISSN - 1524-4539
pISSN - 0009-7322
DOI - 10.1161/01.cir.98.4.346
Subject(s) - glycoprotein 130 , myocyte , leukemia inhibitory factor , transfection , cardiac myocyte , stat protein , stat3 , mapk/erk pathway , medicine , microbiology and biotechnology , signal transduction , biology , janus kinase , endocrinology , cell culture , interleukin 6 , cytokine , genetics
gp130, a signal transducer of the IL-6-related cytokines, is expressed ubiquitously, including in the heart. The activation of gp130 in cardiac myocytes was reported to induce myocardial hypertrophy. The downstream side of gp130 consists of two distinct pathways in cardiac myocytes, one a Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway, the other a mitogen-activated protein kinase (MAPK) pathway. In the present study, we examined whether the JAK/STAT pathway, especially the STAT3-mediated pathway, plays a critical role in gp130-dependent myocardial hypertrophy by transfecting wild-type and mutated-type STAT3 cDNA to cardiac myocytes.
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