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Kinin B1 and B2 receptors are overexpressed in the hippocampus of humans with temporal lobe epilepsy

✍ Scribed by Sandra Regina Perosa; Gustavo Adolfo Argañaraz; Eduardo Massatoshi Goto; Luciana Gilbert Pessoa Costa; Ana Carla Konno; Pedro Paulo Vasconcellos Varella; Joselita Ferreira Carvalho Santiago; João Bosco Pesquero; Mauro Canzian; Debora Amado; Elza Marcia Yacubian; Henrique Carrete Jr.; Ricardo Silva Centeno; Esper Abrão Cavalheiro; Jose Antonio Silva Jr.; Maria da Graça Naffah Mazzacoratti


Publisher
John Wiley and Sons
Year
2006
Tongue
English
Weight
340 KB
Volume
17
Category
Article
ISSN
1050-9631

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✦ Synopsis


Abstract

Molecular biology tools have been employed to investigate the participation of peptides in human temporal lobe epilepsy (TLE). Active polypeptides and their receptors have been related to several brain processes, such as inflammation, apoptosis, brain development, K^+^ and Ca^2+^ channels' activation, cellular growth, and induction of neuronal differentiation. Previous works have shown a neuroprotector effect for kinin B2 receptor and a deleterious, pro‐epileptogenic action for kinin B1 receptor in animal models of TLE. The present work was delineated to analyze the kinin B1 and B2 receptors expression in the hippocampus of patients presenting refractory mesial TLE. The hippocampi were removed during the patients surgery in a procedure used for seizure control and compared with tissues obtained after autopsy. Nissl staining was performed to study the tissue morphology and immunohistochemistry, and Western blot was used to compare the distribution and levels of both receptors in the hippocampus. In addition, real time PCR was employed to analyze the gene expression of these receptors. Nissl staining showed sclerotic hippocampi with hilar, granular, and pyramidal cell loss in TLE patients. Immunohistochemistry and Western blot analyses showed increased expression of kinin B1 and B2 receptors but the real‐time PCR data demonstrated increased mRNA level only for kinin B2 receptors, when compared with controls. These data show for the first time a relationship between human TLE and the kallikrein–kinin system, confirming ours previous results, obtained from experimental models of epilepsy. © 2006 Wiley‐Liss, Inc.


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