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. 2016 Nov;117(11):2496-505.
doi: 10.1002/jcb.25542. Epub 2016 Apr 1.

Suppression of EC-SOD by oxLDL During Vascular Smooth Muscle Cell Proliferation

Junya Makino  1 , Rei Asai  1 , Mao Hashimoto  1 , Tetsuro Kamiya  2 , Hirokazu Hara  1 , Masayuki Ninomiya  3 , Mamoru Koketsu  3 , Tetsuo Adachi  1
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Suppression of EC-SOD by oxLDL During Vascular Smooth Muscle Cell Proliferation

Junya Makino et al. J Cell Biochem. 2016 Nov.

Abstract

Reactive oxygen species (ROS) produced by endothelial cells and macrophages play important roles in atherogenesis because they promote the formation of oxidized low-density lipoproteins (oxLDL). Extracellular-superoxide dismutase (EC-SOD) is mainly produced by vascular smooth muscle cells (VSMCs), is secreted into the extracellular space, and protects cells from the damaging effects of the superoxide anion. Thus, the expression of EC-SOD in VSMCs is crucial for protecting cells against atherogenesis; however, oxLDL-induced changes in the expression of EC-SOD in VSMCs have not yet been examined. We herein showed that oxLDL decreased EC-SOD mRNA and protein levels by binding to lectin-like oxidized LDL receptor-1 (LOX-1). Moreover, we demonstrated the significant role of mitogen-activated protein kinase (MEK)/extracellular-regulated protein kinase (ERK) signaling in oxLDL-elicited reductions in the expression of EC-SOD and proliferation of VSMCs. The results obtained with the FCS treatment indicate that oxLDL-elicited reductions in the expression of EC-SOD are related to the proliferation of VSMCs. We herein showed for the first time that luteolin, a natural product, restored oxLDL-induced decreases in the expression of EC-SOD and proliferation of VSMCs. Collectively, the results of the present study suggest that oxLDL accelerates the development of atherosclerosis by suppressing the expression of EC-SOD and also that luteolin has potential as a treatment for atherosclerosis. J. Cell. Biochem. 117: 2496-2505, 2016. © 2016 Wiley Periodicals, Inc.

Keywords: CELL GROWTH; EXTRACELLULAR-SUPEROXIDE DISMUTASE; LECTIN-LIKE OXIDIZED LDL RECEPTOR-1; MITOGEN-ACTIVATED PROTEIN KINASE; OXIDIZED LOW-DENSITY LIPOPROTEIN.

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