Glioma cell activation by Alzheimer's peptide Abeta1-42, alpha1-antichymotrypsin, and their mixture.

Research output: Contribution to journalArticle

Standard

Glioma cell activation by Alzheimer's peptide Abeta1-42, alpha1-antichymotrypsin, and their mixture. / Sun, Yongxin; Wright, H T; Janciauskiene, Sabina.

In: Cellular and Molecular Life Sciences, Vol. 59, No. 10, 2002, p. 1734-43.

Research output: Contribution to journalArticle

Harvard

APA

CBE

MLA

Vancouver

Author

RIS

TY - JOUR

T1 - Glioma cell activation by Alzheimer's peptide Abeta1-42, alpha1-antichymotrypsin, and their mixture.

AU - Sun, Yongxin

AU - Wright, H T

AU - Janciauskiene, Sabina

PY - 2002

Y1 - 2002

N2 - 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.

AB - 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.

KW - Kinetics

KW - Peptide Fragments: chemical synthesis

KW - Human

KW - Interleukin-6: genetics

KW - DNA Primers

KW - DNA

KW - Neoplastic: drug effects

KW - Glioma: physiopathology

KW - Amyloid beta-Protein: pharmacology

KW - Base Sequence

KW - Amyloid beta-Protein: chemical synthesis

KW - Gene Expression Regulation

KW - Neoplasm: biosynthesis

KW - Gelatinase B: metabolism

KW - Peptide Fragments: pharmacology

KW - RNA

KW - Messenger: genetics

KW - Reverse Transcriptase Polymerase Chain Reaction

KW - Support

KW - Non-U.S. Gov't

KW - Thymidine: metabolism

KW - Transcription

KW - Genetic: drug effects

KW - Tumor Cells

KW - Cultured

KW - Tumor Necrosis Factor: genetics

KW - alpha 1-Antichymotrypsin: pharmacology

U2 - 10.1007/PL00012501

DO - 10.1007/PL00012501

M3 - Article

VL - 59

SP - 1734

EP - 1743

JO - Cellular and Molecular Life Sciences

JF - Cellular and Molecular Life Sciences

SN - 1420-9071

IS - 10

ER -