The renin-angiotensin system is upregulated in the cortex and hippocampus of patients with temporal lobe epilepsy related to mesial temporal sclerosis
Article first published online: 21 MAR 2008
© 2008 International League Against Epilepsy
Volume 49, Issue 8, pages 1348–1357, August 2008
How to Cite
Argañaraz, G. A., Konno, A. C., Perosa, S. R., Santiago, J. F. C., Boim, M. A., Vidotti, D. B., Varella, P. P. V., Costa, L. G., Canzian, M., Porcionatto, M. A., Yacubian, E. M., Sakamoto, A. C., Carrete Jr, H., Centeno, R. S., Amado, D., Cavalheiro, E. A., Junior, J. A. S. and Mazzacoratti, M. d. G. N. (2008), The renin-angiotensin system is upregulated in the cortex and hippocampus of patients with temporal lobe epilepsy related to mesial temporal sclerosis. Epilepsia, 49: 1348–1357. doi: 10.1111/j.1528-1167.2008.01581.x
- Issue published online: 28 JUL 2008
- Article first published online: 21 MAR 2008
- Accepted February 15, 2008; Online Early publicationMarch 21, 2008.
- Angiotensin II AT1 and AT2 receptors;
- Temporal lobe epilepsy;
Purpose: As reported by several authors, angiotensin II (AngII) is a proinflammatory molecule that stimulates the release of inflammatory cytokines and activates nuclear factor κB (NFκB), being also associated with the increase of cellular oxidative stress. Its production depends on the activity of the angiotensin converting enzyme (ACE) that hydrolyzes the inactive precursor angiotensin I (AngI) into AngII. It has been suggested that AngII underlies the physiopathological mechanisms of several brain disorders such as stroke, bipolar disorder, schizophrenia, and disease. The aim of the present work was to localize and quantify AngII AT1 and AT2 receptors in the cortex and hippocampus of patients with temporal lobe epilepsy related to mesial temporal sclerosis (MTS) submitted to corticoamygdalohippocampectomy for seizure control.
Method: Immunohistochemistry, Western blot, and real-time PCR techniques were employed to analyze the expression of these receptors.
Results: The results showed an upregulation of AngII AT1 receptor as well as its messenger ribonucleic acid (mRNA) expression in the cortex and hippocampus of patients with MTS. In addition, an increased immunoexpression of AngII AT2 receptors was found only in the hippocampus of these patients with no changes in its mRNA levels.
Discussion: These data show, for the first time, changes in components of renin-angiotensin system (RAS) that could be implicated in the physiopathology of MTS.