INTERLEUKIN-1-BETA DISSOCIATES BETA-AMYLOID PRECURSOR PROTEIN AND BETA-AMYLOID PEPTIDE SECRETION

被引:28
作者
VASILAKOS, JP [1 ]
CARROLL, RT [1 ]
EMMERLING, MR [1 ]
DOYLE, PD [1 ]
DAVIS, RE [1 ]
KIM, KS [1 ]
SHIVERS, BD [1 ]
机构
[1] NEW YORK STATE INST BASIC RES DEV DISABIL, STATEN ISL, NY 10314 USA
关键词
BETA-AMYLOID PRECURSOR PROTEIN; BETA-AMYLOID PEPTIDE; INTERLEUKIN; 1-BETA; H4; NEUROGLIOMA;
D O I
10.1016/0014-5793(94)01142-7
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
A heightened production of interleukin 1 beta (IL-1 beta) has been reported in microglial-associated amyloid deposits in Alzheimer's disease (AD) brains. These plaques are composed predominantly of beta/A4 peptide derived from beta-amyloid precursor protein (beta APP). We demonstrate that short-term (1 h) IL-1 beta-treatment increases beta APP(s) secretion and concomitantly decreases cell-associated beta APP in human H4 neuroglioma cells. Long-term (5 h) IL-1 beta treatment did not alter secreted or cell-associated beta APP content. In contrast, the secretion of beta/A4-containing epitope was not affected by short-term IL-1 beta stimulation; however, long-term IL-1 beta treatment decreased the amount of beta/A4-containing epitope secreted from the cells. These results show that IL-1 beta modifies the processing and secretion of beta APP to exacerbate perhaps the neuropathology of AD.
引用
收藏
页码:289 / 292
页数:4
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