Differential expression of rat brain Bcl-2 family proteins in development and aging

被引：57

作者：

Shimohama, S ^{[1
]}

Fujimoto, S

Sumida, Y

Tanino, H

机构：

[1] Kyoto Univ, Fac Med, Dept Neurol, Sakyo Ku, Kyoto 606, Japan

[2] Kyoto Pharmaceut Univ, Dept Environm Biochem, Kyoto 607, Japan

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 1998年 / 252卷 / 01期

关键词：

D O I：

10.1006/bbrc.1998.9577

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：

We have previously examined the involvement of the B cell leukemia-2 gene product (Bcl-2) family proteins (Bcl-2, Bcl-x, Bax, Bak, and Bad) in Alzheimer's disease (AD) and found that Bcl-2, Bcl-x, Bak, and Bad were upregulated. As AD is an aging-associated disease, in the present study we examined the developmental and aging-related changes in Bcl-2 family proteins in the rat brain. Immunoblot analyses of brain extracts from embryonic day 19 (E19) to postnatal 96-week-old rats indicated that the Bcl-2 protein level was highest at E19 and decreased after birth. Bcl-x levels remained high from E19 to 96 weeks. Bax levels were high hom E19 to 2 weeks and decreased from 4 weeks onward. Bak levels were highest at E19 and decreased abruptly after birth. Bad levels were high from E19 to 2 weeks and decreased abruptly at 4 weeks. The present results suggest that the expression of each Bcl-2 family protein is differentially regulated during development and aging and that the changes in the senescent brains are different from those observed in AD. (C) 1998 Academic Press.

引用

页码：92 / 96

页数：5

共 23 条

[11] BCL-X IS EXPRESSED IN EMBRYONIC AND POSTNATAL NEURAL TISSUES AND FUNCTIONS TO PREVENT NEURONAL CELL-DEATH [J].

GONZALEZGARCIA, M ;

GARCIA, I ;

DING, LY ;

OSHEA, S ;

BOISE, LH ;

THOMPSON, CB ;

NUNEZ, G .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1995, 92 (10) :4304-4308

[12] BCL-2 INHIBITION OF NEURAL DEATH - DECREASED GENERATION OF REACTIVE OXYGEN SPECIES [J].

KANE, DJ ;

SARAFIAN, TA ;

ANTON, R ;

HAHN, H ;

GRALLA, EB ;

VALENTINE, JS ;

ORD, T ;

BREDESEN, DE .

SCIENCE, 1993, 262 (5137) :1274-1277

[13] ALZHEIMERS-DISEASE [J].

KATZMAN, R .

NEW ENGLAND JOURNAL OF MEDICINE, 1986, 314 (15) :964-973

[14] Alteration of proteins regulating apoptosis, Bcl-2, Bcl-x, Bax, Bak, Bad, ICH-1 and CPP32, in Alzheimer's disease [J].

Kitamura, Y ;

Shimohama, S ;

Kamoshima, W ;

Ota, T ;

Matsuoka, Y ;

Nomura, Y ;

Smith, MA ;

Perry, G ;

Whitehouse, PJ ;

Taniguchi, T .

BRAIN RESEARCH, 1998, 780 (02) :260-269

[15] OVEREXPRESSION OF BCL-2 IN TRANSGENIC MICE PROTECTS NEURONS FROM NATURALLY-OCCURRING CELL-DEATH AND EXPERIMENTAL-ISCHEMIA [J].

MARTINOU, JC ;

DUBOISDAUPHIN, M ;

STAPLE, JK ;

RODRIGUEZ, I ;

FRANKOWSKI, H ;

MISSOTTEN, M ;

ALBERTINI, P ;

TALABOT, D ;

CATSICAS, S ;

PIETRA, C ;

HUARTE, J .

NEURON, 1994, 13 (04) :1017-1030

[16] Life and death of neurons in the aging brain [J].

Morrison, JH ;

Hof, PR .

SCIENCE, 1997, 278 (5337) :412-419

[17] MASSIVE CELL-DEATH OF IMMATURE HEMATOPOIETIC-CELLS AND NEURONS IN BCL-X-DEFICIENT MICE [J].

MOTOYAMA, N ;

WANG, FP ;

ROTH, KA ;

SAWA, H ;

NAKAYAMA, K ;

NEGISHI, I ;

SENJU, S ;

ZHANG, Q ;

FUJII, S ;

LOH, DY .

SCIENCE, 1995, 267 (5203) :1506-1510

[18] Developmental and aging changes of Bak expression in the human brain [J].

Obonai, T ;

Mizuguchi, M ;

Takashima, S .

BRAIN RESEARCH, 1998, 783 (01) :167-170

[19] BCL-2 HETERODIMERIZES IN-VIVO WITH A CONSERVED HOMOLOG, BAX, THAT ACCELERATES PROGRAMMED CELL-DEATH [J].

OLTVAI, ZN ;

MILLIMAN, CL ;

KORSMEYER, SJ .

CELL, 1993, 74 (04) :609-619

[20]

Shimizu S, 1996, ONCOGENE, V12, P2251

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