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

Neuroscience

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

13 Scopus citations

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
State	Published - Dec 16 2002

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.

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

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@article{eca0cb498cd0482aa81ab6277fc865af,

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.",

year = "2002",

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

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T1 - Kainate treatment alters TGF-β3 gene expression in the rat hippocampus

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.

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.

KW - Astrocyte

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KW - Kainic acid

KW - Neurodegeneration

KW - Transforming growth factor-β3

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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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