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

来源：

FEBS LETTERS | 1994年 / 354卷 / 03期

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

页码：289 / 292

页数：4

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