STAT signalling in the mature and aging brain

被引:52
作者
De-Fraja, C
Conti, L
Govoni, S
Battaini, F
Cattaneo, E
机构
[1] Univ Milan, Inst Pharmacol Sci, I-20133 Milan, Italy
[2] Univ Pavia, Inst Pharmacol, Pavia, Italy
[3] Univ Rome Tor Vergata, Dept Neurosci, Rome, Italy
关键词
JAK/STAT; signal transduction; neurons; aging brain;
D O I
10.1016/S0736-5748(00)00007-1
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
Activation of the Janus kinases (JAK) and signal transducers and activator of transcription (STAT) proteins in response to specific cytokines and growth factors has been investigated primarily in cells of non-neuronal origin. More recently, the JAKs and the STATs have also been found to be active in the developing and mature brain, providing evidence for important roles played by these molecules in the control of neuronal proliferation, survival and differentiation. Nothing, however, is known about their occurrence and role(s) in the aged brain. We, therefore, investigated the presence of Stat3 and Stat1 in aged-rat brain, and have found that the Stat3 protein was markedly down regulated with respect to adult tissue, while Stat1 remained invariant. We also investigated the potential role of some growth factors in the activation of the JAK/STAT in mature neurons, exposing primary neuronal cells to ciliary neurotrophic factor (CNTF), basic fibroblast growth factor (bFGF) and epidermal growth factor (EGF). Besides CNTF, which is known to recruit Stat3, we found that Stat3 was also tyrosine phosphorylated by bFGF. These data are indicative of an important role of Stat3 and Stat1 in regulating the physiological status of mature neurons. (C) 2000 ISDN. Published by Elsevier Science Ltd. All rights reserved.
引用
收藏
页码:439 / 446
页数:8
相关论文
共 64 条
[1]   BCL-2 GENE IS HIGHLY EXPRESSED DURING NEUROGENESIS IN THE CENTRAL-NERVOUS-SYSTEM [J].
ABEDOHMAE, S ;
HARADA, N ;
YAMADA, K ;
TANAKA, R .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1993, 191 (03) :915-921
[2]   THE PROTOONCOGENE BCL-2 CAN SELECTIVELY RESCUE NEUROTROPHIC FACTOR-DEPENDENT NEURONS FROM APOPTOSIS [J].
ALLSOPP, TE ;
WYATT, S ;
PATERSON, HF ;
DAVIES, AM .
CELL, 1993, 73 (02) :295-307
[3]   Ciliary neurotrophic factor protects striatal output neurons in an animal model of Huntington disease [J].
Anderson, KD ;
Panayotatos, N ;
Corcoran, TL ;
Lindsay, RM ;
Wiegand, SJ .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1996, 93 (14) :7346-7351
[4]  
Baird Andrew, 1994, Current Opinion in Neurobiology, V4, P78, DOI 10.1016/0959-4388(94)90035-3
[5]   Sealing one's fate: control of cell death in neurons [J].
Bergeron, L ;
Yuan, JY .
CURRENT OPINION IN NEUROBIOLOGY, 1998, 8 (01) :55-63
[6]  
Berhow MT, 1996, J NEUROSCI, V16, P8019
[7]   Regulation of gliogenesis in the central nervous system by the JAK-STAT signaling pathway [J].
Bonni, A ;
Sun, Y ;
NadalVicens, M ;
Bhatt, A ;
Frank, DA ;
Rozovsky, I ;
Stahl, N ;
Yancopoulos, GD ;
Greenberg, ME .
SCIENCE, 1997, 278 (5337) :477-483
[8]   A COMPARISON OF CELL POPULATIONS AT VARIOUS DEPTH LEVELS IN CEREBRAL CORTEX OF YOUNG ADULT AND AGED LONG-EVANS RATS [J].
BRIZZEE, KR ;
SHERWOOD, N ;
TIMIRAS, PS .
JOURNALS OF GERONTOLOGY, 1968, 23 (03) :289-&
[9]  
BRODY H, 1973, DEV AGING NERVOUS SY, P121
[10]  
Cattaneo E, 1998, J NEUROSCI RES, V53, P223, DOI 10.1002/(SICI)1097-4547(19980715)53:2<223::AID-JNR11>3.0.CO