Hydrogen Sulfide Downregulates Oncostatin M Expression via PI3K/Akt/NF-κB Signaling Processes in Neutrophil-like Differentiated HL-60 Cells

• Published in: Antioxidants Vol. 12; no. 2; p. 417
• Main Authors: Han, Na-Ra, Ko, Seong-Gyu, Park, Hi-Joon, Moon, Phil-Dong
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 01.02.2023; MDPI
• Subjects: 1-Phosphatidylinositol 3-kinase; Akt; AKT protein; Cell culture; Cell differentiation; Colony-stimulating factor; Communication; Cytokines; Enzyme-linked immunosorbent assay; Gene expression; Granulocyte-macrophage colony-stimulating factor; Health aspects; Hydrogen sulfide; Immunoblotting; Immunofluorescence; Inflammatory diseases; Ischemia; Kinases; Leukocytes (neutrophilic); neutrophil-like differentiated HL-60 cells; Neutrophils; NF-κB protein; nuclear factor-κB; Observations; Oncostatin M; Osteoarthritis; Oxidative stress; phosphatidylinositol 3-kinase; Phosphorylation; Retinal degeneration; Statistical analysis; Variance analysis; South Korea; United States > US; nuclear factor-κB; oncostatin M; Akt; hydrogen sulfide; neutrophil-like differentiated HL-60 cells; phosphatidylinositol 3-kinase
• ISSN: 2076-3921; 2076-3921
• DOI: 10.3390/antiox12020417

The cytokine oncostatin M (OSM) is regarded as a critical mediator in various inflammatory responses. While the gaseous signaling molecule hydrogen sulfide (H S) plays a role in a variety of pathophysiological conditions, such as hypertension, inflammatory pain, osteoarthritis, ischemic stroke, oxidative stress, retinal degeneration, and inflammatory responses, the underlying mechanism of H S action on OSM expression in neutrophils needs to be clarified. In this work, we studied how H S reduces OSM expression in neutrophil-like differentiated (d)HL-60 cells. To evaluate the effects of H S, sodium hydrosulfide (NaHS, a donor that produces H S), ELISA, real-time PCR (qPCR), immunoblotting, and immunofluorescence staining were utilized. Although exposure to granulocyte-macrophage colony-stimulating factor (GM-CSF) resulted in upregulated levels of production and mRNA expression of OSM, these upregulated levels were reduced by pretreatment with NaHS in dHL-60 cells. Similarly, the same pretreatment lowered phosphorylated levels of phosphatidylinositol 3-kinase, Akt, and nuclear factor-kB that had been elevated by stimulation with GM-CSF. Overall, our results indicated that H S could be a therapeutic agent for inflammatory disorders via suppression of OSM.