Induced expressions of Rab24 GTPase and LC3 in nerve-injured motor neurons

被引:44
作者
Egami, Y
Kiryu-Seo, S
Yoshimori, T
Kiyama, H
机构
[1] Osaka City Univ, Dept Anat & Neurobiol, Grad Sch Med, Abeno Ku, Osaka 5458585, Japan
[2] Natl Inst Genet SOKENDAI, Dept Cell Genet, Mishima, Shizuoka 4118540, Japan
关键词
nerve injury; motor neuron; Rab3A; peripheral nerve; autophagy; survive; rat;
D O I
10.1016/j.bbrc.2005.09.171
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 [生物化学与分子生物学]; 081704 [应用化学];
摘要
Rab24 is a member of the Rab GTPase family, but its function is unclear. Here, we demonstrated increase in Rab24 mRNA in nerve-injured hypoglossal motor neurons of rats. Expression of Rab24 mRNA was also induced in differentiated PC12 cells following proteasome inhibitor (MG132) treatment. MG132 treatment further induced expression of microtubule-associated protein light chain 3 (LC3), and accumulation of LC3-II, a processed form of LC3 and the most reliable marker for autophagy. Induction of LC3 mRNA and accumulation of LC3-II were also observed in nerve-injured hypoglossal motor neurons, and partial co-localization of Rab24 and LC3 was demonstrated by immunohistochemistry. The present data suggest that nerve injury promotes autophagy-like events, and this may be an important response for degradation of unnecessary and misfolded proteins to recycle limited amino acids, and synthesize new proteins that are necessary for survival and nerve regeneration responses. (c) 2005 Elsevier Inc. All rights reserved.
引用
收藏
页码:1206 / 1213
页数:8
相关论文
共 24 条
[1]
In vivo and in vitro characterization of novel neuronal plasticity factors identified following spinal cord injury [J].
Di Giovanni, S ;
De Biase, A ;
Yakovlev, A ;
Finn, T ;
Beers, J ;
Hoffman, EP ;
Faden, AI .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2005, 280 (03) :2084-2091
[2]
Characterization of chronic low-level proteasome inhibition on neural homeostasis [J].
Ding, QX ;
Dimayuga, E ;
Martin, S ;
Bruce-Keller, AJ ;
Nukala, V ;
Cuervo, AM ;
Keller, JN .
JOURNAL OF NEUROCHEMISTRY, 2003, 86 (02) :489-497
[3]
Rab24 is an atypical member of the Rab GTPase family - Deficient GTPase activity, GDP dissociation inhibitor interaction, and prenylation of Rab24 expressed in cultured cells [J].
Erdman, RA ;
Shellenberger, KE ;
Overmeyer, JH ;
Maltese, WA .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2000, 275 (06) :3848-3856
[4]
SSR180575 (7-chloro-N,N,5-trimethyl-4-oxo-3-phenyl-3,5-dihydro-4H-pyridazino[4,5-b]indole-1-acetamide), a peripheral benzodiazepine receptor ligand, promotes neuronal survival and repair [J].
Ferzaz, B ;
Brault, E ;
Bourliaud, G ;
Robert, JP ;
Poughon, G ;
Claustre, Y ;
Marguet, F ;
Liere, P ;
Schumacher, M ;
Nowicki, JP ;
Fournier, J ;
Marabout, B ;
Sevrin, M ;
George, P ;
Soubrie, P ;
Benavides, J ;
Scatton, B .
JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS, 2002, 301 (03) :1067-1078
[5]
Proteasome inhibition induces inclusion bodies associated with intermediate filaments and fragmentation of the Golgi apparatus [J].
Harada, M ;
Kumemura, H ;
Omary, MB ;
Kawaguchi, T ;
Maeyama, N ;
Hanada, S ;
Taniguchi, E ;
Koga, H ;
Suganuma, T ;
Ueno, T ;
Sata, M .
EXPERIMENTAL CELL RESEARCH, 2003, 288 (01) :60-69
[6]
An unfolded putative transmembrane polypeptide, which can lead to endoplasmic reticulum stress, is a substrate of parkin [J].
Imai, Y ;
Soda, M ;
Inoue, H ;
Hattori, N ;
Mizuno, Y ;
Takahashi, R .
CELL, 2001, 105 (07) :891-902
[7]
LC3, a mammalian homologue of yeast Apg8p, is localized in autophagosome membranes after processing [J].
Kabeya, Y ;
Mizushima, N ;
Uero, T ;
Yamamoto, A ;
Kirisako, T ;
Noda, T ;
Kominami, E ;
Ohsumi, Y ;
Yoshimori, T .
EMBO JOURNAL, 2000, 19 (21) :5720-5728
[8]
Kiryu S, 1995, J NEUROSCI, V15, P7872
[9]
Noxa is a critical mediator of p53-dependent motor neuron death after nerve injury in adult mouse [J].
Kiryu-Seo, S ;
Hirayama, T ;
Kato, R ;
Kiyama, H .
JOURNAL OF NEUROSCIENCE, 2005, 25 (06) :1442-1447
[10]
Aggresomes, inclusion bodies and protein aggregation [J].
Kopito, RR .
TRENDS IN CELL BIOLOGY, 2000, 10 (12) :524-530