Interleukin-24 Suppresses the Growth of Vascular Smooth Muscle Cells by Inhibiting H2O2-Induced Reactive Oxygen Species Production
- Authors
- Lee, Ki-Mo; Kang, Haeng-A.; Park, Min; Lee, Hwa-Youn; Song, Min-Ji; Ko, Kisung; Oh, Jae-Wook; Kang, Hyung-Sik
- Issue Date
- Nov-2012
- Publisher
- KARGER
- Keywords
- Cell growth; H2O2; Interleukin-24; Mouse vascular aortic smooth muscle cells; Reactive oxygen species
- Citation
- PHARMACOLOGY, v.90, no.5-6, pp 332 - 341
- Pages
- 10
- Journal Title
- PHARMACOLOGY
- Volume
- 90
- Number
- 5-6
- Start Page
- 332
- End Page
- 341
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/20997
- DOI
- 10.1159/000343242
- ISSN
- 0031-7012
1423-0313
- Abstract
- 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 G(0)/G(1) 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. Copyright (C) 2012 S. Karger AG, Basel
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