Author |
Iores-Marcal, Ligia M.
![]() ![]() Viel, Tania A. ![]() Buck, Hudson Sousa ![]() Nunes, Viviane A. ![]() ![]() Gozzo, Andrezza Justino ![]() ![]() Cruz-Silva, Ilana ![]() ![]() Miranda, Antonio ![]() ![]() Shimamoto, Kazuaki ![]() Ura, Nobuyuki ![]() Araujo, Mariana S. ![]() ![]() |
Institution | Universidade Federal de São Paulo (UNIFESP) Fac Ciencias Med Santa Casa São Paulo Sapporo Med Univ |
Abstract | The kallikrein-kinin system is involved in a variety of physiological and pathological processes. Components of this system, identified in rat and human brains, can be altered in neurodegenerative processes such as Alzheimer's disease. Here, we studied kinin release and its inactivation in rats submitted to chronic cerebroventricular infusion of beta-amyloid (A beta) peptide. Neurodegeneration was confirmed by histological analysis of brain samples. in cerebrospinal fluid of animals infused with A beta, bradykinin concentration was increased, as determined by radioimmunoassay. However, in the brain of A beta group, we only detected the tripeptide Arg-Pro-Pro, purified by reversed-phase chromatography and characterized by liquid chromatography-electrospray ionization mass spectrometry. This fragment of bradykinin indicated the possible participation of kinin-processing enzymes in the brain such as a prolyl oligopeptidase. (c) 2006 Elsevier Inc. All rights reserved. |
Keywords |
beta-amyloid
bradykinin kallikrein-kinin system kininase |
Language | English |
Date | 2006-12-01 |
Published in | Peptides. New York: Elsevier B.V., v. 27, n. 12, p. 3363-3369, 2006. |
ISSN | 0196-9781 (Sherpa/Romeo, impact factor) |
Publisher | Elsevier B.V. |
Extent | 3363-3369 |
Origin |
|
Access rights | Closed access |
Type | Article |
Web of Science ID | WOS:000242821300042 |
URI | http://repositorio.unifesp.br/handle/11600/29299 |
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