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

被引：32

作者：

Lee, Ki-Mo ^{[1
]}

Kang, Haeng-A. ^{[1
]}

Park, Min ^{[1
]}

Lee, Hwa-Youn ^{[1
]}

Choi, Ha-Rim ^{[2
]}

Yun, Chul-Ho ^{[1
]}

Oh, Jae-Wook ^{[3
]}

Kang, Hyung-Sik ^{[1
]}

机构：

[1] Chonnam Natl Univ, Sch Biol Sci & Technol, Kwangju 500757, South Korea

[2] Nambu Univ, Kwangju 506706, South Korea

[3] Konkuk Univ, Coll Anim Biosci & Technol, Div Anim Life Sci, Seoul 143701, South Korea

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2012年 / 428卷 / 01期

关键词：

Calcification; Interleukin-24; Calcification and osteoblastic markers; Wnt/beta-catenin pathway; PHOSPHATE-INDUCED CALCIFICATION; IN-VITRO; CANCER; MINERALIZATION; MECHANISMS; MDA-7/IL-24; PROTEINS; STATINS;

D O I：

10.1016/j.bbrc.2012.09.145

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

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 p-glycerophosphate (beta-GP)-induced rat vascular smooth muscle cell (VSMC) calcification model. In this study, IL-24 significantly inhibited beta-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 beta-GP-induced apoptosis and expression of calcification and osteoblastic markers. In addition, IL-24 abrogated beta-GP-induced activation of the Wnt/beta-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 beta-GP-induced VSMC calcification by inhibiting apoptosis, the expression of calcification and osteoblastic markers, and the Wnt/ beta-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. (C) 2012 Elsevier Inc. All rights reserved.

引用

页码：50 / 55

页数：6

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