Abstract
In Alzheimer's disease (AD), chemotaxis might be responsible for attracting glial cells towards the neuritic plaque. Using primary monocyte-derived macrophages and primary adult astrocytes as a model, amyloid-beta (Abeta) (1-42) was able to stimulate the production, as measured by RT-PCR, of MIP-1alpha and MIP-1beta mRNA in macrophages and MCP-1 in astrocytes. Cocultures showed in unstimulated as well as in Abeta-stimulated cells an increase in MIP-1alpha, MIP-1beta and MCP-1 mRNA. ELISAs of supernatant samples of stimulated macrophages and astrocytes also showed an increase in MIP-1alpha and MIP-1beta in macrophages and MCP-1 in astrocytes. Stimulated cocultures showed an increase in MIP-1alpha, MIP-1beta and MCP-1 protein levels in contrast to unstimulated cocultures.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Adult
-
Alzheimer Disease / immunology
-
Amyloid beta-Peptides / pharmacology*
-
Astrocytes / cytology
-
Astrocytes / drug effects
-
Astrocytes / immunology*
-
Cells, Cultured
-
Chemokine CCL2 / genetics
-
Chemokine CCL3
-
Chemokine CCL4
-
Chemokines / genetics*
-
Chemotaxis, Leukocyte / immunology
-
Coculture Techniques
-
Gene Expression / drug effects
-
Gene Expression / immunology
-
Humans
-
Macrophage Inflammatory Proteins / genetics
-
Macrophages / cytology
-
Macrophages / drug effects
-
Macrophages / immunology*
-
Peptide Fragments / pharmacology*
Substances
-
Amyloid beta-Peptides
-
Chemokine CCL2
-
Chemokine CCL3
-
Chemokine CCL4
-
Chemokines
-
Macrophage Inflammatory Proteins
-
Peptide Fragments
-
amyloid beta-protein (1-40)
-
amyloid beta-protein (1-42)