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Kinin B1 and B2 receptors are overexpressed in the hippocampus of humans with temporal lobe epilepsy
Author(s) -
Perosa Sandra Regina,
Argañaraz Gustavo Adolfo,
Goto Eduardo Massatoshi,
Costa Luciana Gilbert Pessoa,
Konno Ana Carla,
Varella Pedro Paulo Vasconcellos,
Santiago Joselita Ferreira Carvalho,
Pesquero João Bosco,
Canzian Mauro,
Amado Debora,
Yacubian Elza Marcia,
Carrete Henrique,
Centeno Ricardo Silva,
Cavalheiro Esper Abrão,
Silva Jose Antonio,
Mazzacoratti Maria da Graça Naffah
Publication year - 2007
Publication title -
hippocampus
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.767
H-Index - 155
eISSN - 1098-1063
pISSN - 1050-9631
DOI - 10.1002/hipo.20239
Subject(s) - kinin , nissl body , hippocampus , receptor , epilepsy , western blot , immunohistochemistry , temporal lobe , neuroscience , human brain , biology , medicine , pathology , immunology , staining , biochemistry , gene , bradykinin
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.