Kinesin and cytoplasmic dynein in spinal spheroids with motor neuron disease

被引:40
作者
Toyoshima, I
Sugawara, M
Kato, K
Wada, C
Hirota, K
Hasegawa, K
Kowa, H
Sheetz, MP
Masamune, O
机构
[1] Akita Univ, Sch Med, Dept Internal Med, Akita 010, Japan
[2] Akita Red Cross Hosp, Div Neurol, Akita 010, Japan
[3] Kitasato Univ, Sch Med, Dept Neurol, Sagamihara, Kanagawa 228, Japan
[4] Duke Univ, Med Ctr, Dept Cell Biol, Durham, NC 27710 USA
关键词
molecular motor; kinesin; cytoplasmic dynein; motor neuron disease; amyotrophic lateral sclerosis; spheroid;
D O I
10.1016/S0022-510X(98)00137-3
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Kinesin and cytoplasmic dynein are two major molecular motors responsible for fast axonal transport. As visualized by immunohistochemistry with monoclonal antibodies, both motors were found to be distributed throughout the cell bodies, dendrites and axons of motor neurons in normal human spinal cords. Large axonal swellings, spheroids, in the spinal cords of patients with motor neuron disease showed massive accumulation of kinesin co-localized with highly phosphorylated neurofilaments. Of 114 spheroids in five spinal cords, 87% were stained heavily with the three anti-kinesin antibodies used in this study. Cytoplasmic dynein was scarce or absent in most of the spheroids. These findings suggest that kinesin selectively accumulates in the spheroids of motor neuron axons, causing disturbance of the machinery for anterograde fast axonal transport in motor neuron disease. (C) 1998 Elsevier Science B.V. All rights reserved.
引用
收藏
页码:38 / 44
页数:7
相关论文
共 29 条
[1]   KINESIN FAMILY IN MURINE CENTRAL-NERVOUS-SYSTEM [J].
AIZAWA, H ;
SEKINE, Y ;
TAKEMURA, R ;
ZHANG, ZZ ;
NANGAKU, M ;
HIROKAWA, N .
JOURNAL OF CELL BIOLOGY, 1992, 119 (05) :1287-1296
[2]   FAST AXONAL-TRANSPORT IN AMYOTROPHIC-LATERAL-SCLEROSIS - AN INTRAAXONAL ORGANELLE TRAFFIC ANALYSIS [J].
BREUER, AC ;
LYNN, MP ;
ATKINSON, MB ;
CHOU, SM ;
WILBOURN, AJ ;
MARKS, KE ;
CULVER, JE ;
FLEEGLER, EJ .
NEUROLOGY, 1987, 37 (05) :738-748
[3]  
CAJAL SRY, 1928, DEGENERATION REGENER, V2, P198
[4]   PROXIMAL AXONAL ENLARGEMENT IN MOTOR NEURON DISEASE [J].
CARPENTER, S .
NEUROLOGY, 1968, 18 (09) :841-+
[5]  
CHOU SHI-MING, 1965, ACTA NEUROPATHOL, V4, P590
[6]   DEFECTIVE AXONAL-TRANSPORT IN A TRANSGENIC MOUSE MODEL OF AMYOTROPHIC-LATERAL-SCLEROSIS [J].
COLLARD, JF ;
COTE, F ;
JULIEN, JP .
NATURE, 1995, 375 (6526) :61-64
[7]   PROGRESSIVE NEURONOPATHY IN TRANSGENIC MICE EXPRESSING THE HUMAN NEUROFILAMENT HEAVY GENE - A MOUSE MODEL OF AMYOTROPHIC-LATERAL-SCLEROSIS [J].
COTE, F ;
COLLARD, JF ;
JULIEN, JP .
CELL, 1993, 73 (01) :35-46
[8]   NEUROFIBRILLARY AXONAL SWELLINGS AND AMYOTROPHIC LATERAL SCLEROSIS [J].
DELISLE, MB ;
CARPENTER, S .
JOURNAL OF THE NEUROLOGICAL SCIENCES, 1984, 63 (02) :241-250
[9]   DIFFERENTIAL PHOSPHORYLATION IN-VIVO OF CYTOPLASMIC DYNEIN ASSOCIATED WITH ANTEROGRADELY MOVING ORGANELLES [J].
DILLMAN, JF ;
PFISTER, KK .
JOURNAL OF CELL BIOLOGY, 1994, 127 (06) :1671-1681
[10]   VARIANTS OF THE HEAVY NEUROFILAMENT SUBUNIT ARE ASSOCIATED WITH THE DEVELOPMENT OF AMYOTROPHIC-LATERAL-SCLEROSIS [J].
FIGLEWICZ, DA ;
KRIZUS, A ;
MARTINOLI, MG ;
MEININGER, V ;
DIB, M ;
ROULEAU, GA ;
JULIEN, JP .
HUMAN MOLECULAR GENETICS, 1994, 3 (10) :1757-1761