Gene expression profile of SOD1-G93A mouse spinal cord, blood and muscle

被引:11
作者
Saris, Christiaan G. J. [1 ]
Groen, Ewout J. N. [1 ]
Van Vught, Paul W. J. [1 ]
van Es, Michael A. [1 ]
Blauw, Hylke M. [1 ]
Veldink, Jan H. [1 ]
van den Berg, Leonard H. [1 ]
机构
[1] Univ Med Ctr Utrecht, Rudolf Magnus Inst Neurosci, Dept Neurol, NL-3584 CX Utrecht, Netherlands
关键词
SOD1; transgenic animals; RNA; biomarkers; AMYOTROPHIC-LATERAL-SCLEROSIS; MOTOR-NEURON INJURY; SKELETAL-MUSCLE; ATPASE ACTIVITY; BIOMARKERS; DISEASE; SOD1; ALS; MUTATIONS; MODEL;
D O I
10.3109/21678421.2012.749914
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
The exact pathway leading to neuron death and muscle atrophy in amyotrophic lateral sclerosis (ALS) has not yet been elucidated. Gene expression profile of spinal cord, blood and muscle could provide signalling pathways and systemic alterations useful for future biomarker development. In our study we compared whole genome expression profiles of lumbar spinal cord with peripheral blood and tibialis anterior muscle in 16 mutant SOD1-G93A mice and 15 wild-type littermates. In SOD1-G93A mice, 11 genes were significantly differentially expressed in spinal cord, and 16 genes in blood, while much larger transcriptional changes were noted in muscle (1745 genes significant; six overlapping with spinal cord (0.3%)) probably due to muscle atrophy. Overlap with spinal cord was enriched for significant genes in blood (six of 16 overlapping with spinal cord (37.5%)). Three genes were significantly down-regulated in all three tissues, and were closely related to mitochondrial function. Furthermore, clustering the significant genes in spinal cord and in blood, but not in muscle, could identify the SOD1-G93A mice. We conclude that blood gene expression profile overlapped with profile of spinal cord, allowing differentiation of SOD1-G93A mice from wild-type littermates. Blood gene expression profiling may be a promising biomarker for ALS patients.
引用
收藏
页码:190 / 198
页数:9
相关论文
共 50 条
  • [31] Stagnation of glymphatic interstitial fluid flow and delay in waste clearance in the SOD1-G93A mouse model of ALS
    Hirose, Mikako
    Asano, Mito
    Watanabe-Matsumoto, Saori
    Yamanaka, Koji
    Abe, Yoichiro
    Yasui, Masato
    Tokuda, Eiichi
    Furukawa, Yoshiaki
    Misawa, Hidemi
    NEUROSCIENCE RESEARCH, 2021, 171 : 74 - 82
  • [32] The role of mitochondrial quality control in lumbar spinal cords of SOD1-G93A transgenic mice
    Han, Jingzhe
    Song, Xueqin
    Zhu, Jianguo
    Zhang, Xin
    Gao, Juan
    Li, Junxia
    Song, Yanmei
    Wu, Hongran
    Guo, Yansu
    Li, Chunyan
    INTERNATIONAL JOURNAL OF CLINICAL AND EXPERIMENTAL PATHOLOGY, 2016, 9 (10): : 9837 - 9852
  • [33] Increased Orexin Expression Promotes Sleep/Wake Disturbances in the SOD1-G93A Mouse Model of Amyotrophic Lateral Sclerosis
    Liu, Rong
    Sheng, Zhao-Fu
    Cai, Bing
    Zhang, Yong-He
    Fan, Dong-Sheng
    CHINESE MEDICAL JOURNAL, 2015, 128 (02) : 239 - 244
  • [34] Very Early Involvement of Innate Immunity in Peripheral Nerve Degeneration in SOD1-G93A Mice
    Angelini, Daniela Francesca
    De Angelis, Federica
    Vacca, Valentina
    Piras, Eleonora
    Parisi, Chiara
    Nutini, Michele
    Spalloni, Alida
    Pagano, Francesca
    Longone, Patrizia
    Battistini, Luca
    Pavone, Flaminia
    Marinelli, Sara
    FRONTIERS IN IMMUNOLOGY, 2020, 11
  • [35] Compensatory changes in degenerating spinal motoneurons sustain functional sparing in the SOD1-G93A mouse model of amyotrophic lateral sclerosis
    Giusto, Elena
    Codrich, Marta
    de Leo, Gioacchino
    Francardo, Veronica
    Coradazzi, Marino
    Parenti, Rosalba
    Gulisano, Massimo
    Vicario, Nunzio
    Gulino, Rosario
    Leanza, Giampiero
    JOURNAL OF COMPARATIVE NEUROLOGY, 2020, 528 (02) : 231 - 243
  • [36] Increased Orexin Expression Promotes Sleep/Wake Disturbances in the SOD1-G93A Mouse Model of Amyotrophic Lateral Sclerosis
    Liu Rong
    Sheng Zhao-Fu
    Cai Bing
    Zhang Yong-He
    Fan Dong-Sheng
    中华医学杂志英文版, 2015, 128 (02) : 239 - 244
  • [37] Neuroprotective Effects of Genistein in a SOD1-G93A Transgenic Mouse Model of Amyotrophic Lateral Sclerosis
    Zhao, Zichun
    Fu, Jinsheng
    Li, Shiping
    Li, Zhenzhong
    JOURNAL OF NEUROIMMUNE PHARMACOLOGY, 2019, 14 (04) : 688 - 696
  • [38] Neuroprotective Effects of Shenqi Fuzheng Injection in a Transgenic SOD1-G93A Mouse Model of Amyotrophic Lateral Sclerosis
    Sugimoto, Kazuo
    Liu, Jia
    Li, MingXuan
    Song, YueBo
    Zhang, Chi
    Zhai, ZhiGuang
    Gao, Ying
    FRONTIERS IN PHARMACOLOGY, 2021, 12
  • [39] Reducing systemic hypermetabolism by inducing hypothyroidism does not prolong survival in the SOD1-G93A mouse
    Li, Jia
    Paulson, Jill M.
    Ye, Felix D.
    Sung, Minhee
    Hollenberg, Anthony N.
    Rutkove, Seward B.
    AMYOTROPHIC LATERAL SCLEROSIS, 2012, 13 (04): : 372 - 377
  • [40] Defective Neuromuscular Transmission in the SOD1G93A Transgenic Mouse Improves After Administration of Human Umbilical Cord Blood Cells
    Souayah, Nizar
    Coakley, K. M.
    Chen, R.
    Ende, Norman
    McArdle, Joseph J.
    STEM CELL REVIEWS AND REPORTS, 2012, 8 (01) : 224 - 228