Dishevelled-1 (Dvl-1) Protein: a Potential Participant of Oxidative Stress Induced by Selenium Deficiency

被引:3
作者
Zhao, Han-dong [1 ]
Sun, Mei-na [1 ]
Li, Meng-di [1 ]
Li, Feng-lan [1 ]
Li, Hui [1 ]
机构
[1] Harbin Med Univ, Basic Med Sci Coll, Dept Biochem & Mol Biol, Harbin 150081, Peoples R China
关键词
Selenium deficiency; Oxidative stress; Dishevelled-1; protein; Wnt pathway; CATENIN SIGNALING PROTECTS; GLUTATHIONE-PEROXIDASE; INDUCED APOPTOSIS; EPITHELIAL-CELLS; KESHAN-DISEASE; HUMAN HEALTH; IN-VITRO; SELENOPROTEINS; PATHWAY; DAMAGE;
D O I
10.1007/s12011-013-9859-5
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
Oxidative stress induced by selenium deficiency has been shown to be associated with cardiovascular diseases. Nevertheless, the mechanism associated with oxidative stress induced by selenium deficiency is poorly understood. In the present study, 36 weaning C57BL/6 mice were randomly divided into 4 groups as follows: control (n = 9), 4-week selenium deficiency (n = 9), 8-week selenium deficiency (n = 9), and 12-week selenium deficiency (n = 9). The levels of myocardial glutathione peroxidase (GPx), superoxide dismutase (SOD), and malondialdehyde (MDA) were determined by Western blotting or commercial kits. Real-time PCR was performed to detect the mRNA expression of dishevelled-1 (Dvl-1) protein. Western blotting was conducted to evaluate the protein expression levels of Dvl-1 and beta-catenin. Our results demonstrated that the levels of GPx and SOD were significantly reduced, along with an increase in MDA in selenium-deficient mice. Importantly, Dvl-1 and beta-catenin were clearly upregulated under oxidative stress. Collectively, our findings indicate that Dvl-1 may be an underlying participant of oxidative stress induced by selenium deficiency.
引用
收藏
页码:45 / 50
页数:6
相关论文
共 38 条
  • [11] Antioxidant and prooxidant mechanisms in the regulation of redox(y)-sensitive transcription factors
    Haddad, JJ
    [J]. CELLULAR SIGNALLING, 2002, 14 (11) : 879 - 897
  • [12] Wnt/β-catenin signaling:: new (and old) players and new insights
    Huang, He
    He, Xi
    [J]. CURRENT OPINION IN CELL BIOLOGY, 2008, 20 (02) : 119 - 125
  • [13] The effect of DHEA treatment on the oxidative stress and myocardial fibrosis induced by Keshan disease pathogenic factors
    Jia, Chunshu
    Chen, Xiaoliang
    Li, Xiangjun
    Li, Min
    Miao, Chunsheng
    Sun, Bo
    Fan, Zhimin
    Ren, Liqun
    [J]. JOURNAL OF TRACE ELEMENTS IN MEDICINE AND BIOLOGY, 2011, 25 (03) : 154 - 159
  • [14] Klotz LO, 2003, J NUTR, V133, p1448S, DOI 10.1093/jn/133.5.1448S
  • [15] Characterization of mammalian selenoproteomes
    Kryukov, GV
    Castellano, S
    Novoselov, SV
    Lobanov, AV
    Zehtab, O
    Guigó, R
    Gladyshev, VN
    [J]. SCIENCE, 2003, 300 (5624) : 1439 - 1443
  • [16] Wnt-β-catenin Signaling Protects Against Hepatic Ischemia and Reperfusion Injury in Mice
    Lehwald, Nadja
    Tao, Guo-Zhong
    Jang, Kyu Yun
    Sorkin, Michael
    Knoefel, Wolfram T.
    Sylvester, Karl G.
    [J]. GASTROENTEROLOGY, 2011, 141 (02) : 707 - U417
  • [17] Is selenium deficiency really the cause of Keshan disease?
    Lei, Cong
    Niu, Xiaolin
    Ma, Xiangke
    Wei, Jin
    [J]. ENVIRONMENTAL GEOCHEMISTRY AND HEALTH, 2011, 33 (02) : 183 - 188
  • [18] PLATELET GLUTATHIONE-PEROXIDASE ACTIVITY AS AN INDEX OF SELENIUM STATUS IN RATS
    LEVANDER, OA
    DELOACH, DP
    MORRIS, VC
    MOSER, PB
    [J]. JOURNAL OF NUTRITION, 1983, 113 (01) : 55 - 63
  • [19] Effects of different states of oxidative stress on fetal rat alveolar type II epithelial cells in vitro and ROS-induced changes in Wnt signaling pathway expression
    Li, Zhu
    Fang, Fang
    Xu, Feng
    [J]. MOLECULAR MEDICINE REPORTS, 2013, 7 (05) : 1528 - 1532
  • [20] Activation of canonical wnt pathway promotes differentiation of mouse bone marrow-derived MSCs into type II alveolar epithelial cells, confers resistance to oxidative stress, and promotes their migration to injured lung tissue in vitro
    Liu, Ai-ran
    Liu, Le
    Chen, Song
    Yang, Yi
    Zhao, Hong-jie
    Liu, Ling
    Guo, Feng-mei
    Lu, Xiao-min
    Qiu, Hai-bo
    [J]. JOURNAL OF CELLULAR PHYSIOLOGY, 2013, 228 (06) : 1270 - 1283