Induction of suppressor of cytokine signaling-3 in astrocytes of the rat hippocampus following transient forebrain ischemia

Jeong Sun Choi; Yoo Jin Shin; Jung Ho Cha; Ha Young Kim; Jae Youn Choi; Myung Hoon Chun; Mun Yong Lee

doi:10.1016/j.neulet.2008.06.051

Induction of suppressor of cytokine signaling-3 in astrocytes of the rat hippocampus following transient forebrain ischemia

Jeong Sun Choi, Yoo Jin Shin, Jung Ho Cha, Ha Young Kim, Jae Youn Choi, Myung Hoon Chun, Mun Yong Lee

Department of Anatomy

The Catholic University of Korea

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

8 Scopus citations

Abstract

We investigated the spatiotemporal expression of suppressor of cytokine signaling-3 (SOCS-3) in the rat hippocampus following transient forebrain ischemia using in situ hybridization and reverse transcriptase-polymerase chain reaction (RT-PCR) analysis. Messenger RNA for SOCS-3 was constitutively expressed in neurons of the pyramidal cell and granule cell layers in control animals; however, significant induction was detected in reactive astrocytes preferentially located in the CA1 and the dentate hilar regions of the ischemic hippocampus. SOCS-3 mRNA was induced within 3 days of ischemia and maintained for more than 2 weeks. The in situ hybridization data agreed with the semiquantitative RT-PCR analysis. These results demonstrate SOCS-3 induction occurs in reactive astrocytes of the post-ischemic hippocampus, suggesting that SOCS-3 is involved in regulating the astroglial reaction to an ischemic insult.

Original language	English
Pages (from-to)	323-327
Number of pages	5
Journal	Neuroscience Letters
Volume	441
Issue number	3
DOIs	https://doi.org/10.1016/j.neulet.2008.06.051
State	Published - 29 Aug 2008

Bibliographical note

Funding Information:
This research was supported by a grant (M103KV010011-07K2201-01110) from Brain Research Center of the 21st Century Frontier Research Program funded by the Ministry of Science and Technology of Republic of Korea.

Keywords

Hippocampus
Reactive astrocytes
SOCS-3
Transient forebrain ischemia

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10.1016/j.neulet.2008.06.051

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title = "Induction of suppressor of cytokine signaling-3 in astrocytes of the rat hippocampus following transient forebrain ischemia",

abstract = "We investigated the spatiotemporal expression of suppressor of cytokine signaling-3 (SOCS-3) in the rat hippocampus following transient forebrain ischemia using in situ hybridization and reverse transcriptase-polymerase chain reaction (RT-PCR) analysis. Messenger RNA for SOCS-3 was constitutively expressed in neurons of the pyramidal cell and granule cell layers in control animals; however, significant induction was detected in reactive astrocytes preferentially located in the CA1 and the dentate hilar regions of the ischemic hippocampus. SOCS-3 mRNA was induced within 3 days of ischemia and maintained for more than 2 weeks. The in situ hybridization data agreed with the semiquantitative RT-PCR analysis. These results demonstrate SOCS-3 induction occurs in reactive astrocytes of the post-ischemic hippocampus, suggesting that SOCS-3 is involved in regulating the astroglial reaction to an ischemic insult.",

keywords = "Hippocampus, Reactive astrocytes, SOCS-3, Transient forebrain ischemia",

author = "Choi, {Jeong Sun} and Shin, {Yoo Jin} and Cha, {Jung Ho} and Kim, {Ha Young} and Choi, {Jae Youn} and Chun, {Myung Hoon} and Lee, {Mun Yong}",

note = "Funding Information: This research was supported by a grant (M103KV010011-07K2201-01110) from Brain Research Center of the 21st Century Frontier Research Program funded by the Ministry of Science and Technology of Republic of Korea.",

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AU - Choi, Jeong Sun

AU - Shin, Yoo Jin

AU - Cha, Jung Ho

AU - Kim, Ha Young

AU - Choi, Jae Youn

AU - Chun, Myung Hoon

AU - Lee, Mun Yong

N1 - Funding Information: This research was supported by a grant (M103KV010011-07K2201-01110) from Brain Research Center of the 21st Century Frontier Research Program funded by the Ministry of Science and Technology of Republic of Korea.

PY - 2008/8/29

Y1 - 2008/8/29

N2 - We investigated the spatiotemporal expression of suppressor of cytokine signaling-3 (SOCS-3) in the rat hippocampus following transient forebrain ischemia using in situ hybridization and reverse transcriptase-polymerase chain reaction (RT-PCR) analysis. Messenger RNA for SOCS-3 was constitutively expressed in neurons of the pyramidal cell and granule cell layers in control animals; however, significant induction was detected in reactive astrocytes preferentially located in the CA1 and the dentate hilar regions of the ischemic hippocampus. SOCS-3 mRNA was induced within 3 days of ischemia and maintained for more than 2 weeks. The in situ hybridization data agreed with the semiquantitative RT-PCR analysis. These results demonstrate SOCS-3 induction occurs in reactive astrocytes of the post-ischemic hippocampus, suggesting that SOCS-3 is involved in regulating the astroglial reaction to an ischemic insult.

AB - We investigated the spatiotemporal expression of suppressor of cytokine signaling-3 (SOCS-3) in the rat hippocampus following transient forebrain ischemia using in situ hybridization and reverse transcriptase-polymerase chain reaction (RT-PCR) analysis. Messenger RNA for SOCS-3 was constitutively expressed in neurons of the pyramidal cell and granule cell layers in control animals; however, significant induction was detected in reactive astrocytes preferentially located in the CA1 and the dentate hilar regions of the ischemic hippocampus. SOCS-3 mRNA was induced within 3 days of ischemia and maintained for more than 2 weeks. The in situ hybridization data agreed with the semiquantitative RT-PCR analysis. These results demonstrate SOCS-3 induction occurs in reactive astrocytes of the post-ischemic hippocampus, suggesting that SOCS-3 is involved in regulating the astroglial reaction to an ischemic insult.

KW - Hippocampus

KW - Reactive astrocytes

KW - SOCS-3

KW - Transient forebrain ischemia

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ER -

Induction of suppressor of cytokine signaling-3 in astrocytes of the rat hippocampus following transient forebrain ischemia

Abstract

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Keywords

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