Bcl‐2/Bax ratio increase does not prevent apoptosis of glia and granular neurons in patients with temporal lobe epilepsy

Bcl‐2/Bax ratio increase does not prevent apoptosis of glia and granular neurons in patients with temporal lobe epilepsy

Temporal lobe epilepsy (TLE) is usually associated with hippocampal sclerosis (HS), characterized by gliosis and neuronal loss, mainly in the cornus ammonis (CA). Regardless the type of HS, gliosis is associated with neuronal loss. Indeed, glial reactivation seems to induce both neuronal and glial a...

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Published in:Neuropathology Vol. 39; no. 5; pp. 348 - 357
Main Authors: Toscano, Eliana C. de Brito, Vieira, Érica L.M., Portela, Ana C.D.C., Reis, Joice L.J., Caliari, Marcelo V., Giannetti, Alexandre V., Gonçalves, Ana P., Siqueira, José M., Suemoto, Claudia K., Leite, Renata E.P., Nitrini, Ricardo, Teixeira, Antônio L., Rachid, Milene A.
Format: Journal Article
Language:English
Published: Melbourne John Wiley & Sons Australia, Ltd 01-10-2019
Wiley Subscription Services, Inc
Subjects:
Adolescent
Adult
Apoptosis
BAX protein
bcl-2-Associated X Protein - metabolism
Caspase-3
Cell death
Epilepsy
Epilepsy, Temporal Lobe - metabolism
Epilepsy, Temporal Lobe - pathology
Female
Glial fibrillary acidic protein
Gliosis
hippocampal sclerosis
Hippocampus
Histocompatibility antigen HLA
Humans
Immunoreactivity
intrinsic apoptosis
Male
Middle Aged
Neuroglia - metabolism
Neuroglia - pathology
Neuronal-glial interactions
Neurons
Neurons - metabolism
Neurons - pathology
Paraffin
Proteins
Proto-Oncogene Proteins c-bcl-2 - metabolism
Sclerosis
Temporal lobe
temporal lobe epilepsy
temporal lobe epilepsy
gliosis
intrinsic apoptosis
hippocampal sclerosis
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Summary:Temporal lobe epilepsy (TLE) is usually associated with hippocampal sclerosis (HS), characterized by gliosis and neuronal loss, mainly in the cornus ammonis (CA). Regardless the type of HS, gliosis is associated with neuronal loss. Indeed, glial reactivation seems to induce both neuronal and glial apoptosis. Anti‐apoptotic mechanisms are also activated in order to contain the cell death in chronic epilepsy. However, the role of the intrinsic apoptosis pathway in human TLE is unclear, mainly in relation to glial death. The purpose of this study was to evaluate the reactive gliosis areas in parallel with Bcl‐2/Bax ratio and active caspase 3 immunoreactivity in hippocampi of TLE patients in comparison with control hippocampi. We also sought to investigate whether the levels of these markers were correlated with TLE clinical parameters. Paraffin‐embedded sclerotic and control hippocampi were collected for immunohistochemical analyses of glial fibrillary acidic protein (GFAP), human leucocyte antigen DR (HLA‐DR), neuronal nuclei protein (NeuN), Bax, Bcl‐2 and active caspase 3. Sclerotic hippocampi presented higher immunoreactivity areas of GFAP and HLA‐DR than controls, with similar values in HS types 1 and 2. Bcl‐2 protein expression was increased in epileptic hippocampi, while Bax expression was similar to controls. Despite Bcl2/Bax ratio increase, granular neurons and glia exhibited active caspase 3 expression in TLE hippocampi, while controls did not show staining for the same marker. In conclusion, glial and neuronal death is increased in sclerotic hippocampi, independently of HS type, and co‐localized with gliosis. Furthermore, Bcl‐2/Bax ratio increase does not prevent expression of active caspase 3 by glia and granular neurons in TLE.
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ISSN:0919-6544
1440-1789
DOI:10.1111/neup.12592