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

Hyoung Chun Kim; Guoying Bing; Seong Jin Kim; Wang Kee Jhoo; Eun Joo Shin; Myung Bok Wie; Kwang Ho Ko; Won Ki Kim; Kathleen C. Flanders; Shin Geon Choi; Jau Shyong Hong

doi:10.1016/S0169-328X(02)00514-4

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

Hyoung Chun Kim^*
, Guoying Bing
, Seong Jin Kim
, Wang Kee Jhoo
, Eun Joo Shin
, Myung Bok Wie
, Kwang Ho Ko
, Won Ki Kim
, Kathleen C. Flanders
, Shin Geon Choi
, Jau Shyong Hong

^*Corresponding author for this work

Research output: Contribution to journal › Article › peer-review

13 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 language	English
Pages (from-to)	60-70
Number of pages	11
Journal	Molecular Brain Research
Volume	108
Issue number	1-2
DOIs	https://doi.org/10.1016/S0169-328X(02)00514-4
Publication status	Published - 2002 Dec 16
Externally published	Yes

Bibliographical note

Funding Information:
This work was supported by the Brain Korea 21 Project, and by a grant (1998-019-F00050) from Korea Research Foundation, Republic of Korea. Equipment at the Institute of Pharmaceutical Science (Kangwon National University) was used in this study.

Copyright:
Copyright 2005 Elsevier B.V., All rights reserved.

Keywords

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

ASJC Scopus subject areas

Molecular Biology
Cellular and Molecular Neuroscience

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10.1016/S0169-328X(02)00514-4

Cite this

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title = "Kainate treatment alters TGF-β3 gene expression in the rat hippocampus",

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.",

keywords = "Astrocyte, Exogenous TGF-β3, Hippocampus, Kainic acid, Neurodegeneration, Transforming growth factor-β3",

author = "Kim, \{Hyoung Chun\} and Guoying Bing and Kim, \{Seong Jin\} and Jhoo, \{Wang Kee\} and Shin, \{Eun Joo\} and Wie, \{Myung Bok\} and Ko, \{Kwang Ho\} and Kim, \{Won Ki\} and Flanders, \{Kathleen C.\} and Choi, \{Shin Geon\} and Hong, \{Jau Shyong\}",

note = "Funding Information: This work was supported by the Brain Korea 21 Project, and by a grant (1998-019-F00050) from Korea Research Foundation, Republic of Korea. Equipment at the Institute of Pharmaceutical Science (Kangwon National University) was used in this study. Copyright: Copyright 2005 Elsevier B.V., All rights reserved.",

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doi = "10.1016/S0169-328X(02)00514-4",

language = "English",

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AU - Kim, Hyoung Chun

AU - Bing, Guoying

AU - Kim, Seong Jin

AU - Jhoo, Wang Kee

AU - Shin, Eun Joo

AU - Wie, Myung Bok

AU - Ko, Kwang Ho

AU - Kim, Won Ki

AU - Flanders, Kathleen C.

AU - Choi, Shin Geon

AU - Hong, Jau Shyong

N1 - Funding Information: This work was supported by the Brain Korea 21 Project, and by a grant (1998-019-F00050) from Korea Research Foundation, Republic of Korea. Equipment at the Institute of Pharmaceutical Science (Kangwon National University) was used in this study. Copyright: Copyright 2005 Elsevier B.V., All rights reserved.

PY - 2002/12/16

Y1 - 2002/12/16

N2 - 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.

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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KW - Exogenous TGF-β3

KW - Hippocampus

KW - Kainic acid

KW - Neurodegeneration

KW - Transforming growth factor-β3

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U2 - 10.1016/S0169-328X(02)00514-4

DO - 10.1016/S0169-328X(02)00514-4

M3 - Article

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SN - 0169-328X

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JF - Molecular Brain Research

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ER -

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

Abstract

Bibliographical note

Keywords

ASJC Scopus subject areas

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