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    Title: The effect of ferulic acid ethyl ester on leptin-induced proliferation and migration of aortic smooth muscle cells
    Authors: Tsai, Yung-Chieh
    Lee, Yen-Mei
    Hsu, Chih-Hsiung
    Leu, Sy-Ying
    Chiang, Hsiao-Yen
    Yen, Mao-Hsiung
    Cheng, Pao-Yun
    Contributors: 運動管理系
    Keywords: Activated protein-kinases
    Oxidative stress
    In-vivo
    Matrix metalloproteinase-2
    Cardiovascular-disease
    Cdk inhibitors
    Adipose-tissue
    Plasma leptin
    Cyclin D1
    Mechanisms
    Date: 2015-08
    Issue Date: 2016-04-19 19:03:19 (UTC+8)
    Publisher: Nature Publishing Group
    Abstract: Leptin is a peptide hormone, which has a central role in the regulation of body weight; it also exerts many potentially atherogenic effects. Ferulic acid ethyl ester (FAEE) has been approved for antioxidant properties. The aim of this study was to investigate whether FAEE can inhibit the atherogenic effects of leptin and the possible molecular mechanism of its action. Both of cell proliferation and migration were measured when the aortic smooth muscle cell (A10 cell) treated with leptin and/or FAEE. Phosphorylated p44/42MAPK, cell cycle-regulatory protein (for example, cyclin D1, p21, p27), beta-catenin and matrix metalloproteinase-9 (MMP-9) proteins levels were also measured. Results demonstrated that leptin (10, 100 ng ml(-1)) significantly increased the proliferation of cells and the phosphorylation of p44/42MAPK in A10 cells. The proliferative effect of leptin was significantly reduced by the pretreatment of U0126 (0.5 mu M), a MEK inhibitor, in A10 cells. Meanwhile, leptin significantly increased the protein expression of cyclin D1, p21, beta-catenin and decreased the expression of p27 in A10 cells. In addition, leptin (10 ng ml(-1)) significantly increased the migration of A10 cells and the expression of MMP-9 protein. Above effects of leptin were significantly reduced by the pretreatment of FAEE (1 and 10 mu M) in A10 cells. In conclusion, FAEE exerts multiple effects on leptin-induced cell proliferation and migration, including the inhibition of p44/42MAPK phosphorylation, cell cycle-regulatory proteins and MMP-9, thereby suggesting that FAEE may be a possible therapeutic approach to the inhibition of obese vascular disease.
    Relation: Experimental And Molecular Medicine, v.47, e180
    Appears in Collections:[Dept. of Sports Management] Periodical Articles

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