Involvement of suppressor of cytokine signaling-1 in globular adiponectin-induced granulocyte colony-stimulating factor in RAW 264 cell

We previously demonstrated that treatment with a globular type of adiponectin (gAd) induced expression of granulocyte colony-stimulating factor (G-CSF) via the MEK/ERK signaling pathway in a murine macrophage cell line, RAW 264. In the present study, we investigated whether suppressor of cytokine signaling-1 (SOCS1) has roles in the regulation of gAd-induced G-CSF generation. Intracellular G-CSF generation induced by gAd treatment peaked after 10 h and then attenuated. SOCS1 mRNA and protein were expressed at 1 h and 4 h after gAd treatment, respectively. Overexpression of SOCS1 reduced G-CSF generation and phosphorylation of ERK, JNK, and p38 MAPK in gAd-treated cells. While gAd treatment induced the translocation of STAT3 to the nucleus under control conditions, STAT3 stayed in the cytosol when SOCS1 was overexpressed. Additionally, knockdown of SOCS1 by interfering RNA caused levels of G-CSF to continue to rise beyond 10 h after gAd treatment. These results suggest that SOCS1 is involved in providing negative feedback for gAd-induced production of G-CSF.

• We examined roles of SOCS1 on the regulation of gAd-induced G-CSF generation.
• gAd treatment induced SOCS1 mRNA and protein expression.
• Overexpression of SOCS1 reduced gAd-induced G-CSF generation, phosphorylation of MAPKs (ERK, JNK, and p38), and STAT3 translocation to nuclei.
• Knockdown of SOCS1 caused of G-CSF levels to continue to rise beyond 10 h after gAd treatment.