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Am J Physiol Cell Physiol (February 1, 2006). doi:10.1152/ajpcell.00322.2005
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Submitted on July 1, 2005
Accepted on January 23, 2006

ONCOSTATIN M DIFFERENTIALLY REGULATES CXC CHEMOKINES IN MOUSE CARDIAC FIBROBLASTS

Pascal J Lafontant1, Alan R Burns1, Elizabeth Donnachie2, Sandra B Haudek1, C. Wayne Smith2, and Mark L Entman1*

1 Medicine, Baylor College of Medicine, Houston, TX, USA
2 Pediatrics, Baylor College of Medicine, Houston, TX, USA

* To whom correspondence should be addressed. E-mail: mle{at}bcm.tmc.edu.

Ischemia and reperfusion injury in the heart is characterized by marked infiltration of neutrophils in the myocardial interstitial space. Studies in human, canine and murine models reveal 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 mouse OSM can regulate the synthesis and release of macrophage inflammatory protein (MIP-2/CXCL-2), KC/CXCL-1, and LPS-induced chemokine (LIX/CXCL-5), 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, while OSM activates the Janus kinase-signal transducers and activators of transcription (JAK-STAT), and the mitogen activated protein kinase (MAPK) pathways, we demonstrate that the OSM-mediated CXC chemokine release in mCFs is also dependent on the activation of the phosphatidylinositol-3-kinase (PI3-K) pathway.




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