Interleukin-24 attenuates β-glycerophosphate-induced calcification of vascular smooth muscle cells by inhibiting apoptosis, the expression of calcification and osteoblastic markers, and the Wnt/β-catenin pathway

• Published in: Biochemical and biophysical research communications Vol. 428; no. 1; pp. 50 - 55
• Main Authors: Lee, Ki-Mo, Kang, Haeng-A., Park, Min, Lee, Hwa-Youn, Choi, Ha-Rim, Yun, Chul-Ho, Oh, Jae-Wook, Kang, Hyung-Sik
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 09.11.2012
• Subjects: Animal models; Animals; Antibodies; Apoptosis; beta -Glycerophosphoric acid; beta Catenin - metabolism; Biomarkers - metabolism; Calcification; Calcification (ectopic); Calcification and osteoblastic markers; Calcium; Cancer; Cardiovascular diseases; catenin; Cell culture; Cells, Cultured; Glycerophosphates - pharmacology; Humans; Interleukin 24; Interleukins - antagonists & inhibitors; Interleukins - pharmacology; Interleukins - physiology; Male; Muscle, Smooth, Vascular; Osteoblasts; Osteoblasts - metabolism; Rats; Rats, Sprague-Dawley; Smooth muscle; Tumors; Vascular Calcification - chemically induced; Vascular Calcification - metabolism; Vascular Calcification - pathology; Wnt protein; Wnt Proteins - metabolism; Wnt/β-catenin pathway; Calcification; Calcification and osteoblastic markers; Wnt/β-catenin pathway; Interleukin-24
• ISSN: 0006-291X; 1090-2104
• DOI: 10.1016/j.bbrc.2012.09.145

► IL-24 prevents β-glycerophosphate (β-GP)-induced calcification of rat VSMCs. ► IL-24 suppresses the β-GP-induced apoptosis of rat VSMCs. ► IL-24 inhibits the β-GP-induced expression of calcification and osteoblast markers. ► IL-24 inhibits the Wnt/β-catenin pathway in β-GP-induced, calcified VSMCs. Vascular calcification is a hallmark of cardiovascular disease. Interleukin-24 (IL-24) has been known to suppress tumor progression in a variety of human cancers. However, the role of IL-24 in the pathophysiology of diseases other than cancer is unclear. We investigated the role of IL-24 in vascular calcification. IL-24 was applied to a β-glycerophosphate (β-GP)-induced rat vascular smooth muscle cell (VSMC) calcification model. In this study, IL-24 significantly inhibited β-GP-induced VSMC calcification, as determined by von Kossa staining and calcium content. The inhibitory effect of IL-24 on VSMC calcification was due to the suppression of β-GP-induced apoptosis and expression of calcification and osteoblastic markers. In addition, IL-24 abrogated β-GP-induced activation of the Wnt/β-catenin pathway, which plays a key role in the pathogenesis of vascular calcification. The specificity of IL-24 for the inhibition of VSMC calcification was confirmed by using a neutralizing antibody to IL-24. Our results suggest that IL-24 inhibits β-GP-induced VSMC calcification by inhibiting apoptosis, the expression of calcification and osteoblastic markers, and the Wnt/ β-catenin pathway. Our study may provide a novel mechanism of action of IL-24 in cardiovascular disease and indicates that IL-24 is a potential therapeutic agent in VSMC calcification.