Kallikrein 1 is overexpressed by astrocytes in the hippocampus of patients with refractory temporal lobe epilepsy, associated with hippocampal sclerosis

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• 作者：Priscila Santos Rodrigues Simõ ; es^a ; Sandra Regina Perosa^a ; Gustavo Adolfo Argan&#xe3 ; raz^b ; Elza Má ; rcia Yacubian^a ; Henrique Carrete Jr.^c ; Ricardo Silva Centeno^a ; Pedro Paulo Vasconcellos Varella^a ; Joselita Ferreira Carvalho Santiago^a ; Mauro Canzian^d ; Jose Antonio Silva Jr.^e ; Renato Arruda Mortara^f ; Dé ; bora Amado^a ; Esper Abr&#xe3 ; o Cavalheiro^a ; Maria da Graç ; a Naffah Mazzacoratti^a ; ^g ; ^{naffahmazz.nexp@epm.br}
• 关键词：Temporal lobe epilepsy ; Kallikrein 1 ; Kinin receptors ; Astrocytes and neurons
• 刊名：Neurochemistry International
• 出版年：2011
• 出版时间：March 2011
• 年：2011
• 卷：58
• 期：4
• 页码：477-482
• 全文大小：1307 K

文摘

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.