Does ceruloplasmin differential express in the brain of Ts65Dn: a mouse mode of Down syndrome?

被引:0
|
作者
Yu, Bin [1 ,2 ]
Kong, Jing [1 ]
Xing, Baoling [2 ]
Zhu, Ziqiang [2 ]
Zhang, Bin [2 ]
Wang, Qiu-wei [2 ]
Shao, Shi-he [1 ]
机构
[1] Jiangsu Univ, Dept Microbiol, Sch Med Sci & Lab Med, Zhenjiang City 213003, Jiangsu, Peoples R China
[2] Nanjing Med Univ, Changzhou Woman & Children Hlth Hosp, Changzhou City 213003, Jiangsu, Peoples R China
关键词
Down syndrome; Ceruloplasmin; Ts65Dn; Nervous system; ALZHEIMERS-DISEASE; DEMENTIA; COPPER;
D O I
10.1007/s10072-013-1570-y
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
To investigate the expression of CP in Down syndrome (DS) mouse model, we especially observed the changes in neuronal CP. We systematically analyzed the level of CP in Ts65Dn mouse, including serum CP concentration and enzymatic activity, CP mRNA in brain, the expression of CP protein in brain. The applied technologies were ELISA, chemical colorimetry, RT-PCR, immunohistochemistry. Compared with the control group, there were no differences of significance in the concentration, enzymatic activity and unit activity of serum ceruloplasmin. By RT-PCR, we also found there were no significant differences in the level of CP mRNA. The expression of CP was positive in the endochylema of neuronal cells of both the groups, and there were no significant difference between the two groups. Meanwhile, there were no differences in four regions of the brain (cerebral cortex, hippocampus, thalamus and cerebella). Although the neurotoxic effects of CP related to some neurodegenerative diseases, but whether it does so in DS remains to be determined.
引用
收藏
页码:589 / 593
页数:5
相关论文
共 50 条
  • [31] Luteolin induces hippocampal neurogenesis in the Ts65Dn mouse model of Down syndrome
    Zhou, Wen-Bo
    Miao, Zong-Ning
    Zhang, Bin
    Long, Wei
    Zheng, Fang-Xiu
    Kong, Jing
    Yu, Bin
    NEURAL REGENERATION RESEARCH, 2019, 14 (04) : 613 - 620
  • [32] Proteomic analysis of cardiovascular development in the Ts65Dn Down Syndrome mouse model
    Moore, Clara S.
    Kelly, Erik
    Franca, Arianna
    DEVELOPMENTAL BIOLOGY, 2011, 356 (01) : 174 - 175
  • [33] Highly penetrant myeloproliferative disease in the Ts65Dn mouse model of Down syndrome
    Kirsammer, Gina
    Jilani, Sarah
    Liu, Hui
    Davis, Elizabeth
    Gurbuxani, Sandeep
    Le Beau, Michelle M.
    Crispino, John D.
    BLOOD, 2008, 111 (02) : 767 - 775
  • [34] Increased hippocampal epigenetic age in the Ts65Dn mouse model of Down Syndrome
    Ravaioli, Francesco
    Stagni, Fiorenza
    Guidi, Sandra
    Pirazzini, Chiara
    Garagnani, Paolo
    Silvani, Alessandro
    Zoccoli, Giovanna
    Bartesaghi, Renata
    Bacalini, Maria Giulia
    FRONTIERS IN AGING NEUROSCIENCE, 2024, 16
  • [35] Alterations of central noradrenergic transmission in Ts65Dn mouse, a model for Down syndrome
    Dierssen, M
    Vallina, IF
    Baamonde, C
    GarciaCalatayud, S
    Lumbreras, MA
    Florez, J
    BRAIN RESEARCH, 1997, 749 (02) : 238 - 244
  • [36] Hippocampal and cerebellar BDNF levels in the Ts65Dn mouse model of Down syndrome
    Roberson, Robin
    Kuddo, Thea
    Caballero, Madeline
    Horowitz, Kari
    Spong, Catherine Y.
    AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY, 2012, 206 (01) : S320 - S320
  • [37] Synaptic Vesicle Recycling Is Unaffected in the Ts65Dn Mouse Model of Down Syndrome
    Marland, Jamie R. K.
    Smillie, Karen J.
    Cousin, Michael A.
    PLOS ONE, 2016, 11 (01):
  • [38] Quantitative PCR genotyping assay for the Ts65Dn mouse model of Down syndrome
    Liu, DP
    Schmidt, C
    Billings, M
    Davisson, MT
    BIOTECHNIQUES, 2003, 35 (06) : 1170 - +
  • [39] Luteolin induces hippocampal neurogenesis in the Ts65Dn mouse model of Down syndrome
    Wen-Bo Zhou
    Zong-Ning Miao
    Bin Zhang
    Wei Long
    Fang-Xiu Zheng
    Jing Kong
    Bin Yu
    NeuralRegenerationResearch, 2019, 14 (04) : 613 - 620
  • [40] Postnatal lethality and cardiac anomalies in the Ts65Dn Down Syndrome mouse model
    Clara S. Moore
    Mammalian Genome, 2006, 17