Changes in Chemokines and Chemokine Receptors Expression in a Mouse Model of Alzheimer's Disease

被引:27
|
作者
Jorda, Adrian [1 ]
Cauli, Omar [2 ]
Santonja, Jose M. [3 ]
Aldasoro, Martin [1 ]
Aldasoro, Constanza [1 ]
Obrador, Elena [1 ]
Ma Vila, Jose [1 ]
Dolores Mauricio, Ma [1 ]
Iradi, Antonio [1 ]
Guerra-Ojeda, Sol [1 ]
Marchio, Patricia [1 ]
Valles, Soraya L. [1 ]
机构
[1] Univ Valencia, Sch Med, Dept Physiol, Valencia, Spain
[2] Univ Valencia, Fac Surg & Chiropody, Valencia, Spain
[3] Clin Hosp Valencia, Valencia, Spain
来源
关键词
Alzheimer's disease; chemokine receptors; chemotaxis; inflammation; behavior; CENTRAL-NERVOUS-SYSTEM; MULTIPLE-SCLEROSIS; COGNITIVE IMPAIRMENT; PPAR-GAMMA; CELL-DEATH; T-CELLS; BETA; CCR5; BRAIN; INFLAMMATION;
D O I
10.7150/ijbs.26703
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
The amyloid precursor protein plus presenilin-1 (APP/PSI) mice are a frequently-used model for Alzheimer's disease studies (AD). However, the data relevant to which proteins are involved in inflammatory mechanism are not sufficiently well-studied using the AD mouse model. Using behavioral studies, quantitative RT-PCR and Western-blot techniques, significant findings were determined by the expression of proteins involved in inflammation comparing APP/PSI and Wild type mice. Increased GFAP expression could be associated with the elevation in number of reactive astrocytes. IL-3 is involved in inflammation and ABDFI intervenes normally in the transport across cell membranes and both were found up-regulated in APP/PSI mice compared to Wild type mice. Furthermore, CCR5 expression was decreased and both CCL3 and CCL4 chemokines were highly expressed indicating a possible gliosis and probably an increase in chemotaxis from lymphocytes and T cell generation. We also noted for the first time, a CCR8 increase expression with diminution of its CCL1 chemokine, both normally involved in protection from bacterial infection and demyelination. Control of inflammatory proteins will be the next step in understanding the progression of AD and also in determining the mechanisms that can develop in this disease.
引用
收藏
页码:453 / 463
页数:11
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