Kainate treatment alters TGF-β3 gene expression in the rat hippocampus
- Authors
- Kim H.-C.; Bing G.; Kim S.-J.; Jhoo W.-K.; Shin E.-J.; Wie M.B.; Ko K.H.; Kim W.-K.; Flanders K.C.; Choi S.-G.; Hong J.-S.
- Issue Date
- 2002
- Keywords
- Astrocyte; Exogenous TGF-β3; Hippocampus; Kainic acid; Neurodegeneration; Transforming growth factor-β3
- Citation
- Molecular Brain Research, v.108, no.1-2, pp 60 - 70
- Pages
- 11
- Indexed
- SCOPUS
- Journal Title
- Molecular Brain Research
- Volume
- 108
- Number
- 1-2
- Start Page
- 60
- End Page
- 70
- URI
- https://scholarworks.korea.ac.kr/kumedicine/handle/2020.sw.kumedicine/22154
- DOI
- 10.1016/S0169-328X(02)00514-4
- ISSN
- 0169-328X
- Abstract
- In order to evaluate the role of transforming growth factor (TGF)-β3 in the neurodegenerative process, we examined the levels of mRNA and immunocytochemical distribution for TGF-β3 in the rat hippocampus after systemic kainic acid (KA) administration. Hippocampal TGF-β3 mRNA level was reduced 3 h after KA injection. However, the levels of TGF-β3 mRNA were elevated 1 day post-KA and lasted for at least 30 days. A mild TGF-β3 immunoreactivity (TGF-β3-IR) in the Ammon's horn and a moderate TGF-β3-IR in the dentate granule cells were observed in the normal hippocampus. The CA1 and CA3 neurons lost their TGF-β3-IR, while TGF-β3-positive glia-like cells proliferated mainly throughout the CA1 sector and had an intense immunoreactivity at 7, 15 and 30 days after KA. This immunocytochemical distribution of TGF-β3-positive non-neuronal populations was similar to that of glial fibrillary acidic protein (GFAP)-positive cells. Double labeling immunocytochemical analysis demonstrated colocalization of TGF-β3- and GFAP-immunoreactivity in the same cells. These findings suggest a compensatory mechanism of astrocytes for the synthesis of TGF-β3 protein in response to KA-induced neurodegeneration. In addition, exogenous TGF-β3 (5 or 10 ng/i.c.v.) significantly attenuated KA-induced seizures and neuronal damages in a dose-related manner. Therefore, our results suggest that TGF-β3 plays an important role in protective mechanisms against KA-induced neurodegeneration. © 2002 Elsevier Science B.V. All rights reserved.
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Collections - 1. Basic Science > Department of Neuroscience > 1. Journal Articles
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