- J Korean Neurol Assoc. 2003;21(5):513-520.
- "Expression of Complement Regulator Genes in Aβ1-42 Stimulated Human Neuroblastoma Cell"
- Young Sook Choi
- "Department of Pathology and Department of Neurology, College of Medicine, Catholic University of Korea"
- "아밀로이드베타단백(Aβ1-42) 투여 후 신경아세포종의 보체조절유전자 발현"
- 최영숙 , 이광수 김상호
- 가톨릭대학교 의과대학 병리학교실, 가톨릭대학교 의과대학 신경과학교실
- Abstract
- "Background: Endogenous complement inhibitors in the brain may protect against the neuroinflammation in
Alzheimer s disease. Human neuroblastoma cells were stimulated by Aβ1 - 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 μM of Aβ1-42 or 0.5 ng/ml - 5 ng/ml of TNFαor both. Actinomycin D (2.5 μM) or cycloheximide (2.5 μM)
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: Aβ1-42 and TNFαupregulated 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 Aβ1-42 stimulated neuroblastoma cell may contribute to
a host defense mechanism against complement-mediated neuronal cell damage.Key Words: Amyloid beta-protein, C1 inhibitor, Complement factor H, CD59 antigen, Actinomycin, Decay-accelerating"
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