Developmental alteration of nerve injury induced glial cell line-derived neurotrophic factor (GDNF) receptor expression is crucial for the determination of injured motoneuron fate

被引:22
作者
Honma, M
Namikawa, K
Mansur, K
Iwata, T
Mori, N
Iizuka, H
Kiyama, H
机构
[1] Osaka City Univ, Grad Sch Med, Dept Anat & Neurobiol, Abeno Ku, Osaka 5458585, Japan
[2] Asahikawa Med Coll, Dept Anat, Asahikawa, Hokkaido 078, Japan
[3] Asahikawa Med Coll, Dept Dermatol, Asahikawa, Hokkaido 078, Japan
[4] Asahikawa Med Coll, Dept Urol, Asahikawa, Hokkaido 078, Japan
[5] Natl Inst Longev Sci, Dept Mol Genet Res, Aichi, Japan
[6] Japan Sci & Technol, CREST, Kawaguchi, Saitama, Japan
关键词
adenoviral vector; antisense-gene transfer; axotomy-induced neuronal death; GDNF; GFR alpha 1; neuron-specific gene expression;
D O I
10.1046/j.1471-4159.2002.01043.x
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
Axotomy-induced neuronal death occurs in neonatal motoneurons, but not in adult rat. Here we demonstrated that during the course of postnatal development, nerve injury induced down-regulation of the glial cell line-derived neurotrophic factor (GDNF) receptor GFRalpha1 in axotomized hypoglossal motoneurons of rat are gradually converted to the adult up-regulation pattern of response. The compensatory expression of GFRalpha1 specifically in the injured motoneurons of neonates by adenovirus succeeded in rescuing the injured neurons without an application of growth factors. To the contrary, the nuclear antisense RNA for GFRalpha1 expression accelerates the axotomy-induced neuronal death in pups. These findings suggest that the receptor expression response after nerve injury is critical for the determination of injured motoneuron fate.
引用
收藏
页码:961 / 975
页数:15
相关论文
共 37 条
[21]  
NIWA H, 1991, GENE, V108, P193, DOI 10.1016/0378-1119(91)90434-D
[22]   Expression of mRNA for Akt, serine-threonine protein kinase, in the brain during development and its transient enhancement following axotomy of hypoglossal nerve [J].
Owada, Y ;
Utsunomiya, A ;
Yoshimoto, T ;
Kondo, H .
JOURNAL OF MOLECULAR NEUROSCIENCE, 1997, 9 (01) :27-33
[23]   Neuronal cell death [J].
Pettmann, B ;
Henderson, CE .
NEURON, 1998, 20 (04) :633-647
[24]  
POLLIN MM, 1991, DEVELOPMENT, V112, P83
[25]  
ROMANES GJ, 1946, J ANAT, V80, P117
[26]   Enhanced and specific gene expression via tissue-specific production of Cre recombinase using adenovirus vector [J].
Sato, Y ;
Tanaka, K ;
Lee, G ;
Kanegae, Y ;
Sakai, Y ;
Kaneko, S ;
Nakabayashi, H ;
Tamaoki, T ;
Saito, I .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1998, 244 (02) :455-462
[27]   Peripheral but not central axotomy induces changes in Janus kinases (JAK) and signal transducers and activators of transcription (STAT) [J].
Schwaiger, FW ;
Hager, G ;
Schmitt, AB ;
Horvat, A ;
Hager, G ;
Streif, R ;
Spitzer, C ;
Gamal, S ;
Breuer, S ;
Brook, GA ;
Nacimiento, W ;
Kreutzberg, GW .
EUROPEAN JOURNAL OF NEUROSCIENCE, 2000, 12 (04) :1165-1176
[28]   Intracellular signaling pathways activated by neurotrophic factors [J].
Segal, RA ;
Greenberg, ME .
ANNUAL REVIEW OF NEUROSCIENCE, 1996, 19 :463-489
[29]   AXOTOMY-INDUCED NEURONAL DEATH DURING DEVELOPMENT [J].
SNIDER, WD ;
ELLIOTT, JL ;
YAN, Q .
JOURNAL OF NEUROBIOLOGY, 1992, 23 (09) :1231-1246
[30]   THE NGF-INDUCIBLE SCG10 MESSENGER-RNA ENCODES A NOVEL MEMBRANE-BOUND PROTEIN PRESENT IN GROWTH CONES AND ABUNDANT IN DEVELOPING NEURONS [J].
STEIN, R ;
MORI, N ;
MATTHEWS, K ;
LO, LC ;
ANDERSON, DJ .
NEURON, 1988, 1 (06) :463-476