Changes of apoptosis-related proteins in hippocampus of SAM mouse in development and aging

被引：20

作者：

Wu, Yan ^{[1
,2
]}

Zhang, Ai-Qun ^{[3
]}

Wai, Maria S. M. ^{[1
]}

Lai, Helen W. L. ^{[1
]}

Wu, Sheng-Xi ^{[4
]}

Yew, David T. ^{[1
]}

机构：

[1] Chinese Univ Hong Kong, Dept Anat, Shatin, Hong Kong, Peoples R China

[2] Capital Univ Med Sci, Dept Anat, Beijing 100054, Peoples R China

[3] Chinese Peoples Liberat Army Gen Hosp, Inst Hepatobiliary Surg, Beijing 100853, Peoples R China

[4] Fourth Mil Med Univ, Dept Anat, KK Leung Brain Res Ctr, Xian 710032, Peoples R China

来源：

NEUROBIOLOGY OF AGING | 2006年 / 27卷 / 05期

关键词：

SAM; Aging; Caspases; Bcl-2; family; Apoptosis;

D O I：

10.1016/j.neurobiolaging.2005.07.014

中图分类号：

R592 [老年病学]; C [社会科学总论];

学科分类号：

03 ; 0303 ; 100203 ;

摘要：

Expression of Caspase and Bcl-2 proteins was examined in the hippocampus of senescence-accelerated mice (SAM, P8 and R1 strain) from E19 to 16 months of age. Immunoblotting analysis showed no upregulation of pro-apoptotic proteins (caspase-2L, -3, -6, -8, -9, and Bax) with age while all the anti-apoptotic proteins (caspase-2S, Bcl-2, and Bcl-XL) remained unchanged during aging. Terminal dUTP nick end labeling (TUNEL) and electron microscopy on the hippocampus of 3- and 16-month-old SAM revealed very few TUNEL positive cells in both groups. Morphometric study further showed neuronal loss in the hippocampus was not age-related. Our results suggest apoptosis and cell loss are minor events in the hippocampus of SAM mice and are unlikely to be the cause of functional decline during aging in SAM. (C) 2005 Elsevier Inc. All rights reserved.

引用

页码：782.e1 / 782.e10

页数：10

共 38 条

[1] Apoptosis in skeletal myocytes of patients with chronic heart failure is associated with exercise intolerance [J].

Adams, V ;

Jiang, H ;

Yu, JT ;

Möbius-Winkler, S ;

Fiehn, E ;

Linke, A ;

Weigl, C ;

Schuler, G ;

Hambrecht, R .

JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 1999, 33 (04) :959-965

[2]

Adams V, 2001, FRONT BIOSCI-LANDMRK, V6, pD1

[3]

Anglade P, 1997, HISTOL HISTOPATHOL, V12, P603

[4] Blockade of N-methyl-D-aspartate receptor activation suppresses learning-induced synaptic elimination [J].

Bock, J ;

Braun, K .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1999, 96 (05) :2485-2490

[5] The mitochondrial-lysosomal axis theory of aging - Accumulation of damaged mitochondria as a result of imperfect autophagocytosis [J].

Brunk, UT ;

Terman, A .

EUROPEAN JOURNAL OF BIOCHEMISTRY, 2002, 269 (08) :1996-2002

[6] The role of caspase cleavage of tau in Alzheimer disease neuropathology [J].

Cotman, CW ;

Poon, WW ;

Rissman, RA ;

Blurton-Jones, M .

JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY, 2005, 64 (02) :104-112

[7] Apoptosis pathways in cancer and cancer therapy [J].

Debatin, KM .

CANCER IMMUNOLOGY IMMUNOTHERAPY, 2004, 53 (03) :153-159

[8] In vitro activation of CPP32 and Mch3 by Mch4, a novel human apoptotic cysteine protease containing two FADD-like domains [J].

FernandesAlnemri, T ;

Armstrong, RC ;

Krebs, J ;

Srinivasula, SM ;

Wang, L ;

Bullrich, F ;

Fritz, LC ;

Trapani, JA ;

Tomaselli, KJ ;

Litwack, G ;

Alnemri, ES .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1996, 93 (15) :7464-7469

[9] Mitochondrial participation in ischemic and traumatic neural cell death [J].

Fiskum, G .

JOURNAL OF NEUROTRAUMA, 2000, 17 (10) :843-855

[10]

Higuchi K, 1999, METHOD ENZYMOL, V309, P674

← 1 2 3 4 →