ID4 mediates proliferation of astrocytes after excitotoxic damage in the mouse hippocampus.
10.5115/acb.2011.44.2.128
- Author:
Young Sook LEE
1
;
Joon Won KANG
;
Young Ho LEE
;
Dong Woon KIM
Author Information
1. Department of Anatomy, School of Medicine, Chungnam National University, Daejeon, Korea. visnu528@cnu.ac.kr
- Publication Type:Original Article
- Keywords:
ID4;
Astrocytes;
Excitotoxicity;
Kainic acid;
Proliferation
- MeSH:
Adenoviridae;
Animals;
Astrocytes;
Basic Helix-Loop-Helix Transcription Factors;
Brain;
Cell Proliferation;
DNA;
Hippocampus;
Kainic Acid;
Mice;
Neurons;
Proteins
- From:Anatomy & Cell Biology
2011;44(2):128-134
- CountryRepublic of Korea
- Language:English
-
Abstract:
Inhibitor of DNA binding (ID) proteins bind to and inhibit the function of basic helix-loop-helix transcription factors, including those that regulate proliferation and differentiation during development. However, little is known about the role of ID proteins in glial activation under neuropathological conditions. In this study, we evaluated the expression of ID4 following induction of excitotoxic lesions in mouse brain by kainic acid injection. The number of ID4-expressing astrocytes increased in the CA1 layer of the injured hippocampus until 3 days post-lesion. To analyze the effects of ID4 on cell proliferation, primary astrocytes were transduced with recombinant adenovirus expressing GFP-ID4. Overexpression of ID4 led to increased proliferation of astrocytes. These results suggest that ID4 plays a proliferative role in astrocyte activation after excitotoxin-induced hippocampal neuronal death.
