Fibronectin modulation by A beta amyloid peptide (25-35) in cultured astrocytes of newborn rat cortex.
Fibronectin appears to be present in Senile Plaques of Alzheimer's disease brains. These senile or neuritic plaques are surrounded by dystrophic neurites, activated microglia and reactive astrocytes. The purpose of this work was to establish if a direct correlation exists between the production of Fibronectin (FN) by astrocytes and the presence of amyloid, analysing the modification of this protein produced after the treatment of cultured astrocytes with amyloid peptide (25-35). Our data showed that the addition of previously polymerised A beta-peptide to cultured astrocytes induced a marked increase in FN immunoreactivity that is in part dependent on phosphatases 2A or phosphatase 1, since was partially inhibited by okadaic acid. The increased amount of FN did not appear to be associated to any specific single isoform of which are mainly present in the rat brain. Our data suggest that in vivo FN accumulated in senile plaques may be the result, at least in part, of the response of reactive astrocyte to the presence of amyloid peptide. The importance of FN up-regulation in vivo, as part of a 'positive' response of the astrocytes to produce molecules that favours neurite outgrowth, is discussed.
Moreno-Flores
M T
MT
Centro de Biología Molecular Severo Ochoa, CSIC-Universidad Autonoma de Madrid, Cantoblanco-Madrid 28049, Spain.
Martín-Aparicio
E
E
Salinero
O
O
Wandosell
F
F
D017398:Alternative Splicing / Q000502:physiology; D000544:Alzheimer Disease / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D016229:Amyloid beta-Peptides / Q000378:metabolism / Q000494:pharmacology*; D000818:Animals; D000831:Animals, Newborn; D001253:Astrocytes / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology; D002454:Cell Differentiation / Q000187:drug effects / Q000502:physiology*; D048429:Cell Size / Q000187:drug effects / Q000502:physiology; D002478:Cells, Cultured / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D002540:Cerebral Cortex / Q000187:drug effects / Q000378:metabolism* / Q000503:physiopathology; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005353:Fibronectins / Q000235:genetics / Q000378:metabolism*; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D005911:Gliosis / Q000139:chemically induced / Q000378:metabolism / Q000503:physiopathology; D006133:Growth Substances / Q000378:metabolism; D007150:Immunohistochemistry; D016501:Neurites / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D019319:Okadaic Acid / Q000494:pharmacology; D010446:Peptide Fragments / Q000378:metabolism / Q000494:pharmacology*; D058225:Plaque, Amyloid / Q000378:metabolism* / Q000473:pathology; D020033:Protein Isoforms / Q000235:genetics / Q000378:metabolism; D012333:RNA, Messenger / Q000187:drug effects / Q000378:metabolism; D051381:Rats; D014746:Vimentin / Q000378:metabolism
D016229:Amyloid beta-Peptides; D004791:Enzyme Inhibitors; D005353:Fibronectins; D005904:Glial Fibrillary Acidic Protein; D006133:Growth Substances; D010446:Peptide Fragments; D020033:Protein Isoforms; D012333:RNA, Messenger; D014746:Vimentin; C074636:amyloid beta-protein (25-35); D019319:Okadaic Acid