Expression of Complement Regulator Genes in Abeta1-42 Stimulated Human Neuroblastoma Cell
Journal of the Korean Neurological Association
;
: 513-520, 2003.
Artigo
em Coreano
| WPRIM
| ID: wpr-145011
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.
Texto completo:
DisponíveL
Índice:
WPRIM (Pacífico Ocidental)
Assunto principal:
Encéfalo
/
Proteínas do Sistema Complemento
/
Fibrinogênio
/
RNA Mensageiro
/
Genes Reguladores
/
Peptídeos beta-Amiloides
/
Fator de Necrose Tumoral alfa
/
Fator H do Complemento
/
Antígenos CD59
/
Antígenos CD55
Limite:
Humanos
Idioma:
Coreano
Revista:
Journal of the Korean Neurological Association
Ano de publicação:
2003
Tipo de documento:
Artigo
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