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Title: Kallikrein 1 is overexpressed by astrocytes in the hippocampus of patients with refractory temporal lobe epilepsy, associated with hippocampal sclerosis
Authors: Rodrigues Simoes, Priscila Santos [UNIFESP]
Perosa, Sandra Regina [UNIFESP]
Arganaraz, Gustavo Adolfo
Yacubian, Elza Márcia Targas [UNIFESP]
Carrete, Henrique [UNIFESP]
Centeno, Ricardo Silva [UNIFESP]
Vasconcellos Varella, Pedro Paulo [UNIFESP]
Carvalho Santiago, Joselita Ferreira [UNIFESP]
Canzian, Mauro
Silva, Jose Antonio
Mortara, Renato Arruda [UNIFESP]
Amado, Debora [UNIFESP]
Cavalheiro, Esper Abrao [UNIFESP]
Naffah Mazzacoratti, Maria da Graca [UNIFESP]
Universidade Federal de São Paulo (UNIFESP)
Univ Fed Rio Grande do Norte
Universidade de São Paulo (USP)
Univ Nove de Julho
Keywords: Temporal lobe epilepsy
Kallikrein 1
Kinin receptors
Astrocytes and neurons
Issue Date: 1-Mar-2011
Publisher: Elsevier B.V.
Citation: Neurochemistry International. Oxford: Pergamon-Elsevier B.V., v. 58, n. 4, p. 477-482, 2011.
Abstract: Kallikrein 1 (hK1) is a tissue enzyme responsible for kinin release in inflammatory cascade. This study was delineated to study the distribution and the co-localization of hK1 and kinin B1 and B2 receptors with glial and/or neuronal proteins markers, in the hippocampus of patients with refractory temporal lobe epilepsy, associated with hippocampal sclerosis (TLE-HS), comparing with control tissues. Hippocampal levels of KLK1 mRNA were also measured.hK1, kinin B1 and B2 receptors, NeuN and GFAP were analyzed using immunohistochemistry and confocal microscopy and KLK1 mRNA was quantified with real time PCR.Increased expression of hK1 by astrocytes co-localized with GFAP was found, contrasting with kinin B1 and B2 receptors, which were co-localized with NeuN in the sclerotic hippocampus. in addition, KLK1 mRNA was also up-regulated in same tissues.These data suggest an overexpression of kallikrein-kinin system and a neuron-glia interaction in the inflammatory process present in refractory TLE-HS. (C) 2011 Elsevier B.V. All rights reserved.
ISSN: 0197-0186
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