Induction of angiogenesis in the β-amyloid peptide-injected rat hippocampus

被引:32
作者
Zand, L [1 ]
Ryu, JK [1 ]
McLarnon, JG [1 ]
机构
[1] Univ British Columbia, Fac Med, Dept Pharmacol & Therapeut, Vancouver, BC V6T 1Z3, Canada
关键词
Alzheimer's disease beta-amyloid peptide; angiogenesis; astrocytes; inflammation; microglia; VEGF;
D O I
10.1097/00001756-200502080-00011
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Angiogenesis, the formation of new capillary blood vessels, has been studied following the stereotaxic injection of beta-amyloid peptide (Abeta(1-42)) into rat hippocampus. Immunohistochemical analysis for laminin showed that neovascularization was only slightly increased, relative to control, in the hippocampus 1 day post-Abeta(1-42) injection. However, 7 days following peptide injection neovascularization was markedly up-regulated (by 2.2-fold) compared to control. Immunoreactivity for the angiogenic stimulatory agent vascular endothelial growth factor (VEGF) was also significantly increased in the hippocampus 7 days after Abeta(1-42) injection. Double immunofluorescence staining demonstrated that the increased level of VEGF immunoreactivity was localized to both astrocytes and microglia, suggesting inflammatory responses contributed to angiogenesis. The findings of beta-amyloid stimulated angiogenesis and the involvement of peptide-induced inflammatory processes may have relevance to the pathology of Alzheimer's disease. (C) 2005 Lippincott Williams Wilkins.
引用
收藏
页码:129 / 132
页数:4
相关论文
共 20 条
[1]   Angiogenesis in cancer and other diseases [J].
Carmeliet, P ;
Jain, RK .
NATURE, 2000, 407 (6801) :249-257
[2]   New vascular tissue rapidly replaces neural parenchyma and vessels destroyed by a contusion injury to the rat spinal cord [J].
Casella, GTB ;
Marcillo, A ;
Bunge, MB ;
Wood, PM .
EXPERIMENTAL NEUROLOGY, 2002, 173 (01) :63-76
[3]   Neuronal death in the hippocampus is promoted by plasmin-catalyzed degradation of laminin [J].
Chen, ZL ;
Strickland, S .
CELL, 1997, 91 (07) :917-925
[4]   Is Alzheimer's disease a neurodegenerative or a vascular disorder? Data, dogma, and dialectics [J].
de la Torre, JC .
LANCET NEUROLOGY, 2004, 3 (03) :184-190
[5]   Alzheimer disease as a vascular disorder - Nosological evidence [J].
de la Torre, JC .
STROKE, 2002, 33 (04) :1152-1162
[6]   The codependence of angiogenesis and chronic inflammation [J].
Jackson, JR ;
Seed, MP ;
Kircher, CH ;
Willoughby, DA ;
Winkler, JD .
FASEB JOURNAL, 1997, 11 (06) :457-465
[7]   Amyloid β peptide-induced corpus callosum damage and glial activation in vivo [J].
Jantaratnotai, N ;
Ryu, JK ;
Kim, SU ;
McLarnon, JG .
NEUROREPORT, 2003, 14 (11) :1429-1433
[8]   Vascular endothelial growth factor in Alzheimer's disease and experimental cerebral ischemia [J].
Kalaria, RN ;
Cohen, DL ;
Premkumar, DRD ;
Nag, S ;
LaManna, JC ;
Lust, WD .
MOLECULAR BRAIN RESEARCH, 1998, 62 (01) :101-105
[9]   Inhibition of endogenous VEGF impedes revascularization and astroglial proliferation: roles for VEGF in brain repair [J].
Krum, JM ;
Khaibullina, A .
EXPERIMENTAL NEUROLOGY, 2003, 181 (02) :241-257
[10]   MICROANGIOPATHY AND THE COLOCALIZATION OF HEPARAN-SULFATE PROTEOGLYCAN WITH AMYLOID IN SENILE PLAQUES OF ALZHEIMERS-DISEASE [J].
PERLMUTTER, LS ;
CHUI, HC ;
SAPERIA, D ;
ATHANIKAR, J .
BRAIN RESEARCH, 1990, 508 (01) :13-19