Temporal and regional expression of Fos-related proteins in response to ischemic injury

被引：20

作者：

Butler, TL ^{[1
]}

Pennypacker, KR ^{[1
]}

机构：

[1] Univ S Florida, Coll Med, Dept Pharmacol & Therapeut, Tampa, FL 33612 USA

来源：

BRAIN RESEARCH BULLETIN | 2004年 / 63卷 / 01期

关键词：

FRA-2; c-Fos; AP-1; MCAO; stroke; neuroprotection;

D O I：

10.1016/j.brainresbull.2003.12.005

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

The AP-1 transcription factor family has been widely studied in the response to ischemic brain injury. The data to date have demonstrated a complex involvement that depends on stimulus, subunit composition and brain region. One member in particular, the Fos-related antigen FRA-2, has demonstrated a potential for controlling neuroprotective gene expression. This study characterized the temporal and regional expression of a variety of proteins following ischemic injury induced by occlusion of the middle cerebral artery in rats. The results demonstrated upregulation of both c-Fos and FRA-2 in penumbral regions that preceded upregulation of the classic injury-associated proteins expressed by astrocytes and microglia and, in the case of FRA-2, appeared to correlate with neuronal survival. A further, previously undescribed, expression of FRA-2 in endothelial cells of the core ischemic region was also demonstrated. (C) 2004 Elsevier Inc. All rights reserved.

引用

页码：65 / 73

页数：9

共 49 条

[11] A C-JUN DOMINANT-NEGATIVE MUTANT PROTECTS SYMPATHETIC NEURONS AGAINST PROGRAMMED CELL-DEATH [J].

HAM, J ;

BABIJ, C ;

WHITFIELD, J ;

PFARR, CM ;

LALLEMAND, D ;

YANIV, M ;

RUBIN, LL .

NEURON, 1995, 14 (05) :927-939

[12] The c-Jun transcription factor - Bipotential mediator of neuronal death, survival and regeneration [J].

Herdegen, T ;

Skene, P ;

Bahr, M .

TRENDS IN NEUROSCIENCES, 1997, 20 (05) :227-231

[13] Inducible and constitutive transcription factors in the mammalian nervous system: control of gene expression by Jun, Fos and Krox, and CREB/ATF proteins [J].

Herdegen, T ;

Leah, JD .

BRAIN RESEARCH REVIEWS, 1998, 28 (03) :370-490

[14] Relationship between metabolic dysfunctions, gene responses and delayed cell death after mild focal cerebral ischemia in mice [J].

Hermann, DM ;

Kilic, E ;

Hata, R ;

Hossmann, KA ;

Mies, G .

NEUROSCIENCE, 2001, 104 (04) :947-955

[15] MOLECULAR-BIOLOGY OF VERTEBRATE LEARNING - IS C-FOS A NEW BEGINNING [J].

KACZMAREK, L .

JOURNAL OF NEUROSCIENCE RESEARCH, 1993, 34 (04) :377-381

[16] DYNAMIC CHANGES IN THE COMPOSITION OF THE AP-1 TRANSCRIPTION FACTOR DNA-BINDING ACTIVITY IN RAT-BRAIN FOLLOWING KAINATE-INDUCED SEIZURES AND CELL-DEATH [J].

KAMINSKA, B ;

FILIPKOWSKI, RK ;

ZURKOWSKA, G ;

LASON, W ;

PRZEWLOCKI, R ;

KACZMAREK, L .

EUROPEAN JOURNAL OF NEUROSCIENCE, 1994, 6 (10) :1558-1566

[17] ELEVATED AP-1 TRANSCRIPTION FACTOR DNA-BINDING ACTIVITY AT THE ONSET OF FUNCTIONAL PLASTICITY DURING DEVELOPMENT OF RAT SENSORY CORTICAL AREAS [J].

KAMINSKA, B ;

MOSIENIAK, G ;

GIERDALSKI, M ;

KOSSUT, M ;

KACZMAREK, L .

MOLECULAR BRAIN RESEARCH, 1995, 33 (02) :295-304

[18]

Kaminska B, 2000, ACTA NEUROBIOL EXP, V60, P395, DOI 10.55782/ane-2000-1358

[19] BIPHASIC EXPRESSION OF THE FOS AND JUN FAMILIES OF TRANSCRIPTION FACTORS FOLLOWING TRANSIENT FOREBRAIN ISCHEMIA IN THE RAT - EFFECT OF HYPOTHERMIA [J].

KAMME, F ;

CAMPBELL, K ;

WIELOCH, T .

EUROPEAN JOURNAL OF NEUROSCIENCE, 1995, 7 (10) :2007-2016

[20] Temporary changes of the AP-1 transcription factor binding activity in the gerbil hippocampus after transient global ischemia, and ischemic tolerance induction [J].

Kapinya, K ;

Penzel, R ;

Sommer, C ;

Kiessling, M .

BRAIN RESEARCH, 2000, 872 (1-2) :282-293

← 1 2 3 4 5 →