Abstract
We compared the effects of Alzheimer’s peptide
(Ab1–42), a1-antichymotrypsin (ACT) and an ACT/Ab1–42
mixture on human glioma DK-MG cells. The solution of
Ab (5 mM) formed by 2-h incubation at room temperature
induced tumour necrosis factor-a (TNF-a) and interleukin
(IL)-6 levels by 55 and 45%, respectively, and increased
gelatinase B activity by 67%, while exposure of
cells to the ACT/Ab1–42 mixture (1:10 molar ratio ACT:
Ab1–42) under the same experimental conditions showed
no effect on IL-6 levels or gelatinase B activity, but
strongly induced TNF-a (by 190%), compared to the con-
CMLS, Cell. Mol. Life Sci. 59 (2002) 1734–1743
1420-682X/02/101734-11
© Birkhäuser Verlag, Basel, 2002 CMLS Cellular and Molecular Life Sciences
trols. Stimulation of the cells with Ab1–42 alone, but not
with ACT, increased by about 20% low-density lipoprotein
(LDL) uptake and mRNA levels for LDL receptor and
HMG-CoA reductase, while the ACT/Ab1–42 mixture significantly
increased LDL uptake (by 50%), up-regulated
mRNA levels for LDL receptor and HMG-CoA reductase
by 48 and 63%, respectively, and increased lipid accumulation
by about 20-fold. These data suggest a possible new
role for Ab in Alzheimer’s disease through its interaction
with the inflammatory reactant, ACT.
(Ab1–42), a1-antichymotrypsin (ACT) and an ACT/Ab1–42
mixture on human glioma DK-MG cells. The solution of
Ab (5 mM) formed by 2-h incubation at room temperature
induced tumour necrosis factor-a (TNF-a) and interleukin
(IL)-6 levels by 55 and 45%, respectively, and increased
gelatinase B activity by 67%, while exposure of
cells to the ACT/Ab1–42 mixture (1:10 molar ratio ACT:
Ab1–42) under the same experimental conditions showed
no effect on IL-6 levels or gelatinase B activity, but
strongly induced TNF-a (by 190%), compared to the con-
CMLS, Cell. Mol. Life Sci. 59 (2002) 1734–1743
1420-682X/02/101734-11
© Birkhäuser Verlag, Basel, 2002 CMLS Cellular and Molecular Life Sciences
trols. Stimulation of the cells with Ab1–42 alone, but not
with ACT, increased by about 20% low-density lipoprotein
(LDL) uptake and mRNA levels for LDL receptor and
HMG-CoA reductase, while the ACT/Ab1–42 mixture significantly
increased LDL uptake (by 50%), up-regulated
mRNA levels for LDL receptor and HMG-CoA reductase
by 48 and 63%, respectively, and increased lipid accumulation
by about 20-fold. These data suggest a possible new
role for Ab in Alzheimer’s disease through its interaction
with the inflammatory reactant, ACT.
| Original language | English |
|---|---|
| Pages (from-to) | 1734-43 |
| Journal | Cellular and Molecular Life Sciences |
| Volume | 59 |
| Issue number | 10 |
| DOIs | |
| Publication status | Published - 2002 |
Subject classification (UKÄ)
- Cell Biology
Free keywords
- Kinetics
- Peptide Fragments: chemical synthesis
- Human
- Interleukin-6: genetics
- DNA Primers
- DNA
- Neoplastic: drug effects
- Glioma: physiopathology
- Amyloid beta-Protein: pharmacology
- Base Sequence
- Amyloid beta-Protein: chemical synthesis
- Gene Expression Regulation
- Neoplasm: biosynthesis
- Gelatinase B: metabolism
- Peptide Fragments: pharmacology
- RNA
- Messenger: genetics
- Reverse Transcriptase Polymerase Chain Reaction
- Support
- Non-U.S. Gov't
- Thymidine: metabolism
- Transcription
- Genetic: drug effects
- Tumor Cells
- Cultured
- Tumor Necrosis Factor: genetics
- alpha 1-Antichymotrypsin: pharmacology
