Abstract
Oncostatin M (OSM) is essential in a wide range of inflammatory responses, and most OSM is produced by neutrophils in respiratory diseases. While resveratrol (RES) is regarded as an anti-inflammatory agent in a variety of conditions, the mechanism of OSM inhibition by RES in neutrophils remains to be elucidated. In this study, we investigated whether RES could inhibit OSM production in neutrophil-like differentiated (d)HL-60 cells. The effects of RES were measured by means of an enzyme-linked immunosorbent assay, real-time polymerase chain reaction, and Western blotting. Increases in production and mRNA expression of OSM resulted from the addition of granulocyte-macrophage colony-stimulating factor (GM-CSF) in neutrophil-like dHL-60 cells; however, these increases were downregulated by RES treatment. Exposure to GM-CSF led to elevations of phosphorylation of phosphatidylinositol 3-kinase (PI3K), Akt, and nuclear factor (NF)-kB. Treatment with RES induced downregulation of the phosphorylated levels of PI3K, Akt, and NF-κB in neutrophil-like dHL-60 cells. These results suggest that RES could be applicable to prevent and/or treat inflammatory disorders through blockade of OSM.
Highlights
Oncostatin M (OSM) is known as a cancer-associated cytokine that is highly expressed in patients with tumors [1,2]
Cytokine OSM plays a role in various pathophysiologic conditions, such as cancer progression, extracellular matrix reconstruction, hemopoiesis, liver regeneration, heart remodeling, and inflammatory reactions [2,6,7,8,9]
Pothoven and colleagues [12] suggested that OSM is produced mainly in neutrophils in respiratory inflammatory disorders
Summary
Oncostatin M (OSM) is known as a cancer-associated cytokine that is highly expressed in patients with tumors [1,2]. Cytokine OSM plays a role in various pathophysiologic conditions, such as cancer progression, extracellular matrix reconstruction, hemopoiesis, liver regeneration, heart remodeling, and inflammatory reactions [2,6,7,8,9]. OSM plays a role in a wide range of inflammatory responses [2]. OSM is involved in respiratory inflammatory disorders, including allergic rhinitis and asthma [11,12]. Treatment with OSM protein enhanced inflammatory responses in human intestinal stromal cell line CCD-18Co cells [3]. It was reported that OSM stimulation elevates inflammatory reactions in human keratinocyte cell line HaCaT cells [13]. Pothoven and colleagues [12] suggested that OSM is produced mainly in neutrophils in respiratory inflammatory disorders. There are no reports that provide a mechanism for OSM
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