Serum amyloid A is present in the capillaries and microinfarcts of hypertensive monkey brain:: an immunohistochemical study

被引:6
作者
Bartolák-Suki, E
Sipe, JD
Fine, RE
Rosene, DL
Moss, MB
机构
[1] Boston Univ, Sch Med, Dept Neurobiol & Anat, Boston, MA 02118 USA
[2] Boston Univ, Sch Med, Dept Biochem, Boston, MA 02118 USA
来源
AMYLOID-JOURNAL OF PROTEIN FOLDING DISORDERS | 2000年 / 7卷 / 02期
关键词
microglia; myelin; endothelium; cognitive decline; inflammation;
D O I
10.3109/13506120009146247
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
Serum amyloid A (SAA) is a major inducible acute phase protein characterized as a transient injury specific constituent of high density lipoprotein. We investigated whether the acute phase SAA (A-apoSAA), as a marker of inflammation, is present in the brain of monkeys with surgically induced hypertension of 39 months duration. Sections from brains of normotensive monkeys (systolic blood pressure<124 mmHg) and hypertensive monkeys (systolic blood pressure>185 mmHg) were processed for immunohistochemistry with a rabbit polyclonal antiserum to human A-apoSAA. We found that A-apoSAA was present in hypertensive but not in normotensive brain sections. Staining was localized to capillary endothelial cells and occasionally to the entire vessel wall of the prefrontal cortex. Staining was also observed in the capillaries and in medium size vessels of the corona radiata, the head of the caudate and, to a smaller extent, in the putamen. Additionally, the A-apoSAA was present in cells forming a circular configuration within microinfarcts. These findings suggest that high blood pressure in the brain can result in either local production of A-apoSAA in the capillaries and within microinfarcts or uptake of A-apoSAA from the blood.
引用
收藏
页码:111 / 117
页数:7
相关论文
共 49 条
[1]  
ALDOBENSON MA, 1982, J IMMUNOL, V128, P2390
[2]   SERUM AMYLOID-A IS A CHEMOATTRACTANT - INDUCTION OF MIGRATION, ADHESION, AND TISSUE INFILTRATION OF MONOCYTES AND POLYMORPHONUCLEAR LEUKOCYTES [J].
BADOLATO, R ;
WANG, JM ;
MURPHY, WJ ;
LLOYD, AR ;
MICHIEL, DF ;
BAUSSERMAN, LL ;
KELVIN, DJ ;
OPPENHEIM, JJ .
JOURNAL OF EXPERIMENTAL MEDICINE, 1994, 180 (01) :203-209
[3]   MODULATION OF ENDOTOXIC ACTIVITY OF LIPOPOLYSACCHARIDE BY HIGH-DENSITY-LIPOPROTEIN [J].
BAUMBERGER, C ;
ULEVITCH, RJ ;
DAYER, JM .
PATHOBIOLOGY, 1991, 59 (06) :378-383
[4]   THE HUMAN ACUTE-PHASE SERUM AMYLOID-A GENE FAMILY - STRUCTURE, EVOLUTION AND EXPRESSION IN HEPATOMA-CELLS [J].
BETTS, JC ;
EDBROOKE, MR ;
THAKKER, RV ;
WOO, P .
SCANDINAVIAN JOURNAL OF IMMUNOLOGY, 1991, 34 (04) :471-482
[5]  
BOULOUMINE A, 1997, HYPERTENSION, V30, P1628
[6]   AUTOCRINE INDUCTION OF COLLAGENASE BY SERUM AMYLOID A-LIKE AND BETA-2-MICROGLOBULIN LIKE PROTEINS [J].
BRINCKERHOFF, CE ;
MITCHELL, TI ;
KARMILOWICZ, MJ ;
KLUVEBECKERMAN, B ;
BENSON, MD .
SCIENCE, 1989, 243 (4891) :655-657
[7]   Alterations of nitric oxide synthase expression with aging and hypertension in rats [J].
Chou, TC ;
Yen, MH ;
Li, CY ;
Ding, YA .
HYPERTENSION, 1998, 31 (02) :643-648
[8]  
CHU CJ, 1997, CHIN MED J TAPAI, V59, P145
[9]   UNTREATED BLOOD-PRESSURE LEVEL IS INVERSELY RELATED TO COGNITIVE-FUNCTIONING - THE FRAMINGHAM-STUDY [J].
ELIAS, MF ;
WOLF, PA ;
DAGOSTINO, RB ;
COBB, J ;
WHITE, LR .
AMERICAN JOURNAL OF EPIDEMIOLOGY, 1993, 138 (06) :353-364
[10]  
Eriksen N., 1993, ACUTE PHASE PROTEINS, P93