Open AccessOncostatin M differentially regulates CXC chemokines in mouse cardiac fibroblasts
Author(s) -
Pascal J. Lafontant,
Alan R. Burns,
Elizabeth Donnachie,
Sandra B. Haudek,
C. Wayne Smith,
Mark L. Entman
Publication year - 2006
Publication title -
ajp cell physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.432
H-Index - 181
eISSN - 1522-1563
pISSN - 0363-6143
DOI - 10.1152/ajpcell.00322.2005
Subject(s) - oncostatin m , cxcl1 , cxcl2 , chemokine , cxc chemokine receptors , cxcl5 , microbiology and biotechnology , cytokine , signal transduction , mapk/erk pathway , chemistry , cardioprotection , receptor , medicine , immunology , biology , ischemia , interleukin 6 , chemokine receptor
Ischemia-reperfusion injury in the heart is characterized by marked infiltration of neutrophils in the myocardial interstitial space. Studies in human, canine, and murine models have revealed oncostatin M (OSM) expression in infiltrating leukocytes. In an effort to assess possible roles of OSM in the myocardium, we used cardiac fibroblasts (mCFs) isolated from adult mouse heart to determine whether recombinant murine OSM regulates the synthesis and release of MIP2/CXCL2, KC/CXCL1, and LIX/CXCL5, which are three potent neutrophil chemoattractants in the mouse. Our results demonstrate that mCFs express OSM receptors and that, within the IL-6 cytokine family, OSM uniquely induces significant release of KC and LIX in mCFs. In addition, although OSM activates the JAK-signal transducers and activators of transcription and MAPK pathways, we demonstrate that the OSM-mediated CXC chemokine release in mCFs is also dependent on the activation of the phosphatidylinositol 3-kinase pathway.
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