Reactive Oxygen Species Production, Expression of Complement Regulator Genes and Phagocytosis in the Murine Microglial Cell after Administration of Beta-Amyloid(A beta1-42) Protein.
- Author:
Young Sook CHOI
1
;
Kwang Soo LEE
;
Sang Ho KIM
Author Information
1. Department of Pathology, The Catholic University of Korea College of Medicine, Seoul, Korea. complt@catholic.ac.kr
- Publication Type:Original Article
- Keywords:
Amyloid beta-protein;
C1 inhibitor;
Microglia;
Phagocytosis;
Reactive oxygen species;
Superoxide dismutase
- MeSH:
Alzheimer Disease;
Amyloid;
Amyloid beta-Peptides;
Animals;
Cell Line;
Clusterin;
Complement Factor H;
Complement System Proteins*;
Genes, Regulator*;
Mice;
Microglia;
Phagocytosis*;
Phagosomes;
Plaque, Amyloid;
Reactive Oxygen Species*;
RNA, Messenger;
Superoxide Dismutase;
Vitronectin
- From:Journal of the Korean Neurological Association
2005;23(1):88-95
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Microglia is a primary cellular component of neuritic plaques in Alzheimer's disease. Beta amyloid deposits attract microglia and activate them to produce inflammatory mediators. The objectives of this study were to characterize activation of the microglia; production of reactive oxygen species (ROS), constitutive and upregulated expression of complement regulators, and intracellular localization of amyloid by phagocytosis. METHODS: BV-2 cells, mouse microglia cell line, were incubated for 3~18 hours with a single dose of 20 micro M of aggregated A beta1-42. ROS measurement was done with FACScan. Messenger RNA expressions of C1-INH, vitronectin, CD59, clusterin, factor H, and superoxide dismutase (SOD) were detected by RT-PCR. The intensity of bands from 6% polyacrylamide electrophoretic gel was analyzed by a bioimage analyzer. The intracellular localization of A beta in the phagocytosed microglia was observed by transmission electron microscope. RESULTS: A beta1-42 activates microglia with an increase of ROS production. Expression of mRNA for SOD was also increased. Messenger RNA for C1-INH and vitronectin were upregulated. A beta fibrils were located in the phagosome of microglia. CONCLUSIONS: A beta activated microglia are playing dual roles as effector and scavenger cell, which as a result, may contribute to the chronic neuroinflammation of Alzheimer's disease.
