Abstract
Oncostatin M (OSM) plays a role in various inflammatory reactions, and neutrophils are the main source of OSM in pulmonary diseases. However, there is no evidence showing the mechanism of OSM production in neutrophils. While dexamethasone (Dex) has been known to exert anti-inflammatory activity in various fields, the precise mechanisms of OSM downregulation by Dex in neutrophils remain to be determined. Here, we examined how OSM is produced in neutrophil-like differentiated HL-60 cells. Enzyme-linked immunosorbent assay, real-time polymerase chain reaction, and Western blot analysis were utilized to assess the potential of Dex. Granulocyte-macrophage colony-stimulating factor (GM-CSF) stimulation resulted in OSM elevation in neutrophil-like dHL-60 cells. OSM elevation induced by GM-CSF is regulated by phosphatidylinositol 3-kinase (PI3K)/Akt/nuclear factor (NF)-kB signal cascades. GM-CSF stimulation upregulated phosphorylated levels of PI3K or Akt or NF-κB in neutrophil-like dHL-60 cells. Treatment with Dex decreased OSM levels as well as the phosphorylated levels of PI3K or Akt or NF-κB in neutrophil-like dHL-60 cells. Our findings show the potential of Dex in the treatment of inflammatory diseases via blocking of OSM.
Highlights
Oncostatin M (OSM) was found in supernatants of phorbol 12-myristate 13-acetate (PMA)-treated U-937 monocyte cell line for the first time in 1986 and decreased the growth of A375 melanoma cells and other tumor cells, but not normal fibroblasts [1]
When we stimulated neutrophil-like differentiated HL-60 neutrophil-like cells (dHL-60) cells with Granulocyte-macrophage colony-stimulating factor (GM-CSF), production levels of OSM were elevated (Figure 1a)
We investigated when the production levels of OSM reach their peak in neutrophil-like dHL-60 cells
Summary
Oncostatin M (OSM) was found in supernatants of phorbol 12-myristate 13-acetate (PMA)-treated U-937 monocyte cell line for the first time in 1986 and decreased the growth of A375 melanoma cells and other tumor cells, but not normal fibroblasts [1]. OSM is implicated in a wide range of physiologic and pathologic processes, including remodeling of the extracellular matrix, hematopoiesis, growth modulation of tumor and non-tumor cells, liver regeneration, cardiac remodeling, and inflammatory reactions [5,6]. It plays a role in various inflammatory reactions. Cytokine OSM is involved in inflammation in rheumatoid arthritis and liver inflammation in hepatocarcinogenesis [7,8]. OSM is implicated in inflammatory pulmonary diseases, such as allergic rhinitis and asthma [9,10]
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