%0 Generic %A K.-M., Lee %A H.-A., Kang %A M., Park %A H.-Y., Lee %A M.-J., Song %A K., Ko %A J.-W., Oh %A H.-S., Kang %D 2012 %T Supplementary Material for: Interleukin-24 Suppresses the Growth of Vascular Smooth Muscle Cells by Inhibiting H2O2-Induced Reactive Oxygen Species Production %U https://karger.figshare.com/articles/dataset/Supplementary_Material_for_Interleukin-24_Suppresses_the_Growth_of_Vascular_Smooth_Muscle_Cells_by_Inhibiting_H_sub_2_sub_O_sub_2_sub_-Induced_Reactive_Oxygen_Species_Production/5124148 %R 10.6084/m9.figshare.5124148.v1 %2 https://karger.figshare.com/ndownloader/files/8710441 %K Cell growth %K H2O2 %K Interleukin-24 %K Mouse vascular aortic smooth muscle cells %K Reactive oxygen species %X Background/Aim: The abnormal growth of vascular smooth muscle cells (VSMCs) induced by reactive oxygen species (ROS) is considered a major pathogenic process in vascular diseases. Interleukin (IL)-24 specifically inhibits cancer cell growth through the induction of cell cycle arrest and apoptosis. However, the role of IL-24 in ROS-induced VSMC growth has not yet been investigated. Methods: An MTT assay, gene expression analysis, flow cytometry and a scratch wound healing assay were performed to determine the anti-growth effects of IL-24 in H2O2-treated mouse vascular aortic smooth muscle (MOVAS) cells. To elucidate the effect of IL-24 on ROS-induced signaling, Western blot analysis was employed. Results: IL-24 inhibited the growth of normal MOVAS cells treated with H2O2 by inducing a cell cycle arrest at the G₀/G1 phase through the regulation of p21 and cyclin D1. Furthermore, IL-24 suppressed mRNA expression of vascular endothelial growth factor and platelet-derived growth factor and subsequently decreased the level of cell migration in response to H2O2. Interestingly, IL-24 attenuated the H2O2-induced ROS production by reducing the mitochondrial H2O2 production and enhancing the expression of antioxidant enzymes. We also showed that the ability of H2O2 to induce the PI3K/Akt and Erk signaling pathways was blocked by IL-24. Conclusion: These findings suggest a novel mechanism in which IL-24 suppresses the growth of normal VSMCs by inhibiting H2O2-induced ROS production through the regulation of mitochondrial ROS production and expression of antioxidant enzymes. %I Karger Publishers