Induction of Bis, a Bcl-2-binding protein, in reactive astrocytes of the rat hippocampus following kainic acid-induced seizure.
- Author:
Mun Yong LEE
1
;
Seong Yun KIM
;
Jeong Sun CHOI
;
Yun Sik CHOI
;
Mi Hee JEON
;
Jung Hee LEE
;
In Kyung KIM
;
Jeong Hwa LEE
Author Information
1. Department of Anatomy, College of Medicine, The Catholic University of Korea, Seoul. leejh@catholic.ac.kr
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- MeSH:
Animals;
Apoptosis;
Astrocytes/*metabolism;
Blotting, Western;
Carrier Proteins/*biosynthesis;
Disease Models, Animal;
Epilepsy, Temporal Lobe/chemically induced/*metabolism;
Fluorescent Antibody Technique;
Hippocampus/*metabolism/pathology;
Kainic Acid;
Male;
Neurons/physiology;
Protein Binding;
Proto-Oncogene Proteins c-bcl-2/metabolism;
Rats;
Rats, Sprague-Dawley
- From:Experimental & Molecular Medicine
2002;34(2):167-171
- CountryRepublic of Korea
- Language:English
-
Abstract:
The expression of Bis (also called Bag-3), a Bcl-2-binding protein, was investigated in the rat kainic acid (KA) model of temporal lobe epilepsy. Western blot analysis showed a significant increase in the expression levels of Bis protein in the hippocampus following the systemic administration of KA. Bis immunoreactivity increased preferentially in the CA1 and CA3 regions, as well as in the hilar region of the dentate gyrus. Experiments with double immunofluorescence revealed that, in KA-administered rats, the cells expressing Bis were GFAP-expressing reactive astrocytes. The increase in Bis immunoreactivity was accompanied by increased Bcl-2 in reactive astrocytes in the striatum radiatum, whereas Bcl-2 immunoreactivity in pyramidal neurons was not affected. These results of the co-expression of Bis and Bcl-2 in reactive astrocytes in this seizure model suggest that Bis might modulate the glial reaction under excitotoxic brain injury, probably by interacting with Bcl-2.
