Human amylin mimics amyloid beta protein-induced reactive gliosis and inhibition of cellular redox activity in cultured astrocytes.
We have previously found that Alzheimer's disease amyloid beta protein (A beta) induces reactive gliosis and inhibits cellular redox activity of astrocytes. In the present study, human amylin, an amyloidogenic peptide with primary sequence dissimilar to A beta, mimicked the effects of A beta in cultured astrocytes. However, the non-amyloidogenic rat amylin showed no effect. These results suggest that amyloidogenic property is important for A beta to induce morphological and functional changes of astrocytes.
Abe
K
K
Department of Chemical Pharmacology, Faculty of Pharmaceutical Sciences, University of Tokyo, Japan.
Kato
M
M
Saito
H
H
D000682:Amyloid / Q000494:pharmacology*; D016229:Amyloid beta-Peptides / Q000502:physiology*; D000818:Animals; D001253:Astrocytes / Q000187:drug effects* / Q000201:enzymology; D004305:Dose-Response Relationship, Drug; D005333:Fetus / Q000166:cytology; D005911:Gliosis / Q000139:chemically induced*; D006801:Humans; D058228:Islet Amyloid Polypeptide; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D010084:Oxidation-Reduction; D051381:Rats; D017208:Rats, Wistar
D000682:Amyloid; D016229:Amyloid beta-Peptides; D058228:Islet Amyloid Polypeptide; D007770:L-Lactate Dehydrogenase