Abstract
Alzheimer's disease is characterized by the presence of senile plaques in the brain composed primarily of amyloid-beta peptide. Microglia have been reported to surround these Abeta plaques, which have opposite roles, provoking a microglia-mediated inflammatory response that contributes to neuronal cell loss or the removal of Abeta and damaged neurons. We herein analyzed the process of expression of Matrix metalloproteinases induced by Abeta stimulation. We found that Abeta1-42 induces a high level of MMP3, MMP12 and MMP13 in the microglia. The signal transduction pathway for the expression of these MMPs mRNA induced by Abeta1-42 depends on PI3K/Akt.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Alzheimer Disease / metabolism
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Amyloid beta-Peptides / pharmacology*
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Animals
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Base Sequence
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Cells, Cultured
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DNA Primers / genetics
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Enzyme Induction / drug effects
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Humans
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Matrix Metalloproteinase 12 / biosynthesis
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Matrix Metalloproteinase 12 / genetics
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Matrix Metalloproteinase 13 / biosynthesis
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Matrix Metalloproteinase 13 / genetics
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Matrix Metalloproteinase 3 / biosynthesis
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Matrix Metalloproteinase 3 / genetics
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Matrix Metalloproteinases / biosynthesis*
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Matrix Metalloproteinases / genetics
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Mice
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Microglia / drug effects*
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Microglia / enzymology*
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Peptide Fragments / pharmacology*
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Phosphatidylinositol 3-Kinases / metabolism
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Proto-Oncogene Proteins c-akt / metabolism
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RNA, Messenger / genetics
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RNA, Messenger / metabolism
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Signal Transduction / drug effects
Substances
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Amyloid beta-Peptides
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DNA Primers
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Peptide Fragments
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RNA, Messenger
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amyloid beta-protein (1-42)
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Phosphatidylinositol 3-Kinases
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Proto-Oncogene Proteins c-akt
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Matrix Metalloproteinase 13
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Matrix Metalloproteinases
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Mmp13 protein, mouse
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Matrix Metalloproteinase 3
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Mmp3 protein, mouse
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Matrix Metalloproteinase 12