Expression of Complement Regulator Genes in Abeta1-42 Stimulated Human Neuroblastoma Cell.
- Author:
Young Sook CHOI
1
;
Kwang Soo LEE
;
Sang Ho KIM
Author Information
1. Department of Pathology, College of Medicine, Catholic University of Korea, Korea. complt@cmc.cuk.ac.kr
- Publication Type:Original Article
- Keywords:
Amyloid beta-protein;
C1 inhibitor;
Complement factor H;
CD59 antigen;
Actinomycin;
Decay-accelerating factor
- MeSH:
Alzheimer Disease;
Amyloid beta-Peptides;
Antigens, CD46;
Antigens, CD55;
Antigens, CD59;
Brain;
Clusterin;
Complement Factor H;
Complement System Proteins*;
Cycloheximide;
Dactinomycin;
Fibrinogen;
Genes, Regulator*;
Humans*;
Neuroblastoma*;
Neurons;
RNA, Messenger;
Tumor Necrosis Factor-alpha
- From:Journal of the Korean Neurological Association
2003;21(5):513-520
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Endogenous complement inhibitors in the brain may protect against the neuroinflammation in Alzheimer's disease. Human neuroblastoma cells were stimulated by Abeta1 - 4 2 to investigate whether the expression of various complement regulator genes is upregulated. METHODS: SK-N-SH cells were incubated overnight with a single dose of 20 microM of Abeta1-42 or 0.5 ng/ml - 5 ng/ml of TNFalpha or both. Actinomycin D (2.5 microM) or cycloheximide (2.5 microM) was also added to the cell suspension. Messenger RNA expression of decay accelerating factor (DAF), membrane cofactor protein (MCP), CD59, complement-receptor 1(CR1), C1 inhibitor (C1-INH), C4-binding protein, factor H, factor I, clusterin and S-protein was measured by RT-PCR. RESULTS: Abeta1-42 and TNFalpha upregulated the expression of C1- INH significantly but increased expression of mRNA for factor H was not statistically significant. The expression of mRNAs for DAF and MCP was at low a level after stimulation. Factor I, CD59 and clusterin were not changed in their mRNA level. The mRNAs for S-protein, C4-binding protein and CR1 were not detected. Actinomycin D suppressed mRNA levels of C1-INH and CD59 significantly. Cycloheximide also inhibited the expression of both C1-INH and CD59. CONCLUSIONS: Early upregulated expression of C1-INH in Abeta1-42 stimulated neuroblastoma cell may contribute to a host defense mechanism against complement-mediated neuronal cell damage.
