Kainate treatment alters TGF-β3 gene expression in the rat hippocampus

Hyoung Chun Kim, Guoying Bing, Seong J. Kim, Wang K. Jhoo, Eun J. Shin, Myung Bok Wie, Kwang H. Ko, Won-Ki Kim, Kathleen C. Flanders, Shin Geon Choi, Jau Shyong Hong

Research output: Contribution to journalArticle

11 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)60-70
Number of pages11
JournalMolecular Brain Research
Volume108
Issue number1-2
DOIs
Publication statusPublished - 2002 Dec 16
Externally publishedYes

Fingerprint

Kainic Acid
Transforming Growth Factors
Hippocampus
Gene Expression
Therapeutics
Glial Fibrillary Acidic Protein
Messenger RNA
Neuroglia
Astrocytes
Seizures

Keywords

  • Astrocyte
  • Exogenous TGF-β3
  • Hippocampus
  • Kainic acid
  • Neurodegeneration
  • Transforming growth factor-β3

ASJC Scopus subject areas

  • Molecular Biology
  • Cellular and Molecular Neuroscience

Cite this

Kim, H. C., Bing, G., Kim, S. J., Jhoo, W. K., Shin, E. J., Wie, M. B., ... Hong, J. S. (2002). Kainate treatment alters TGF-β3 gene expression in the rat hippocampus. Molecular Brain Research, 108(1-2), 60-70. https://doi.org/10.1016/S0169-328X(02)00514-4

Kainate treatment alters TGF-β3 gene expression in the rat hippocampus. / Kim, Hyoung Chun; Bing, Guoying; Kim, Seong J.; Jhoo, Wang K.; Shin, Eun J.; Wie, Myung Bok; Ko, Kwang H.; Kim, Won-Ki; Flanders, Kathleen C.; Choi, Shin Geon; Hong, Jau Shyong.

In: Molecular Brain Research, Vol. 108, No. 1-2, 16.12.2002, p. 60-70.

Research output: Contribution to journalArticle

Kim, HC, Bing, G, Kim, SJ, Jhoo, WK, Shin, EJ, Wie, MB, Ko, KH, Kim, W-K, Flanders, KC, Choi, SG & Hong, JS 2002, 'Kainate treatment alters TGF-β3 gene expression in the rat hippocampus', Molecular Brain Research, vol. 108, no. 1-2, pp. 60-70. https://doi.org/10.1016/S0169-328X(02)00514-4
Kim, Hyoung Chun ; Bing, Guoying ; Kim, Seong J. ; Jhoo, Wang K. ; Shin, Eun J. ; Wie, Myung Bok ; Ko, Kwang H. ; Kim, Won-Ki ; Flanders, Kathleen C. ; Choi, Shin Geon ; Hong, Jau Shyong. / Kainate treatment alters TGF-β3 gene expression in the rat hippocampus. In: Molecular Brain Research. 2002 ; Vol. 108, No. 1-2. pp. 60-70.
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AU - Wie, Myung Bok

AU - Ko, Kwang H.

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AU - Choi, Shin Geon

AU - Hong, Jau Shyong

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AB - 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.

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